Article

Gut microbiota: An underestimated and unintended recipient for pesticide-induced toxicity

Authors:
To read the full-text of this research, you can request a copy directly from the authors.

Abstract

Pesticide pollution residues have become increasingly common health hazards over the last several decades because of the wide use of pesticides. The gastrointestinal tract is the first physical and biological barrier to contaminated food and is therefore the first exposure site. Interestingly, a number of studies have shown that the gut microbiota plays a key role in the toxicity of pesticides and has a profound relationship with environmental animal and human health. For instance, intake of the pesticide of chlorpyrifos can promote obesity and insulin resistance through influencing gut and gut microbiota of mice. In this review, we discussed the possible effects of different kinds of widely used pesticides on the gut microbiota in different experimental models and analyzed their possible subsequent effects on the health of the host. More and more studies indicated that the gut microbiota of animals played a very important role in pesticides-induced toxicity, suggesting that gut micriobita was also the unintended recipient of pesticides. We hope that more attention can focus on the relationship between pesticides, gut microbiota and environmental health risk assessment in near future.

No full-text available

Request Full-text Paper PDF

To read the full-text of this research,
you can request a copy directly from the authors.

... Thus, perturbations or dysbiosis of the gut microbiota can lead to increased susceptibility to infections and survival risks at the individual and colony level and serve as a sensitive indicator of xenobiotic-induced stress (Botina et al., 2019). Recent evidence has suggested that the gut microbiota may be correlated with the detoxification of pesticides (Giambò et al., 2021;Yuan et al., 2019) and some pollutants, such as microplastics (Wang et al., 2021). There is growing interest in the interactions between gut microbiota and host metabolic homeostasis. ...
... The gut microbial community in the intestinal system is closely linked to pesticide-induced toxicity in humans and other animals, including insects such as bees (Yuan et al., 2019). Previous studies have shown that permethrin reduces the abundance of Bacteroides, Prevotella, and Porphyromonas and increases the abundance of Enterobacteriaceae and Lactobacillus in rats (Nasuti et al., 2016;Yuan et al., 2019). ...
... The gut microbial community in the intestinal system is closely linked to pesticide-induced toxicity in humans and other animals, including insects such as bees (Yuan et al., 2019). Previous studies have shown that permethrin reduces the abundance of Bacteroides, Prevotella, and Porphyromonas and increases the abundance of Enterobacteriaceae and Lactobacillus in rats (Nasuti et al., 2016;Yuan et al., 2019). Yang et al. (2019) Saccharibacter were significantly affected. ...
Article
Flumethrin is one of the few acaricides that permit the control of Varroa disease or varroosis in bee colonies. However, flumethrin accumulates in hive products. We previously discovered that sublethal doses of flumethrin induce significant physiological stress in honeybees (Apis mellifera L.), however its potential impacts on the honeybee gut microenvironment remains unknown. To fill this gap, honeybees were exposed to a field-relevant concentration of flumethrin (10 μg/L) for 14 d and its potential impacts on gut system were evaluated. The results indicated that flumethrin triggered immune responses in the gut but had limited effects on survival and gut microbial composition. However, survival stress drastically increased in bees exposed to antibiotics, suggesting that the gut microbiota is closely related to flumethrin-induced dysbiosis in the bee gut. Based on a non-targeted metabolomics approach, flumethrin at 10 μg/L considerably altered the composition of intestinal metabolites, and we discovered that this metabolic stress was closely linked with a reduction of gut core bacterial endosymbiont Gilliamella spp. through a combination of microbiological and metabolomics investigations. Finally, an in vitro study showed that while flumethrin does not directly inhibit the growth of Gilliamella apicola isolates, it does have a significant impact on the glycerophospholipid metabolism in bacteria cells, which was also observed in host bees. These findings indicated that even though flumethrin administered at environmental relevant concentrations does not significantly induce death in honeybees, it still alters the metabolism balance between honeybees and the gut symbiotic bacterium, G. apicola. The considerable negative impact of flumethrin on the honeybee gut microenvironment emphasizes the importance of properly monitoring acaricide to avoid potential environmental concerns, and further studies are needed to illustrate the mode of action of bee health-gut microbiota-exogenous pesticides.
... For example, most studies on wild animals have shown that diet in terms of prey species has a large effect on the microbial community composition [2,[5][6][7]. Other factors such as exposure to pollutants have been also shown to have an influence on host-microbiota [8][9][10][11][12][13]. Despite knowledge on the effects of prey consumption on the consumer's host-microbiota, we know little about the potential carry-over effects of pollutants across trophic levels in predator-prey interactions. ...
... We predicted: (1) an increase in the abundance of certain groups of microbes and decrease of diversity of the host-microbiome due to the exposure to MPs; MPs would behave as substrates for the microbial community, decreasing microbial diversity and increasing microbial abundance in functional digestion-related phyla such as Proteobacteria and Firmicutes [40,49,50]. (2) In the presence of DMT, we predicted a negative effect on the microbial diversity and abundance due to the pesticide bactericidal activity, affecting phyla such a Bacteroidetes that might be involved in gut barrier functions [13,50]. (3) In the combined exposure to MPs and DMT, we predicted that the MPs might exert a sequestering effect on the pesticide by adsorption, resulting on lower effects on the diversity and abundance of the microbiome compared to separate effects of MPs or DMT alone. ...
... with the most abundant phyla found in D. magna in the present study. In vertebrates, a decrease of Bacteroidetes might be related to abnormal intestinal permeability and pro-obesity phenotype [8,13,78]. The observed significant effect of Proteobacteria and Bacteroidetes in our experiment by the exposure to MPs and DMT supports our first and second predictions. ...
Article
Full-text available
Background Microplastics are a pervasive pollutant widespread in the sea and freshwater from anthropogenic sources, and together with the presence of pesticides, they can have physical and chemical effects on aquatic organisms and on their microbiota. Few studies have explored the combined effects of microplastics and pesticides on the host–microbiome, and more importantly, the effects across multiple trophic levels. In this work, we studied the effects of exposure to microplastics and the pesticide deltamethrin on the diversity and abundance of the host–microbiome across a three-level food chain: daphnids–damselfly–dragonflies. Daphnids were the only organism exposed to 1 µm microplastic beads, and they were fed to damselfly larvae. Those damselfly larvae were exposed to deltamethrin and then fed to the dragonfly larvae. The microbiotas of the daphnids, damselflies, and dragonflies were analyzed. Results Exposure to microplastics and deltamethrin had a direct effect on the microbiome of the species exposed to these pollutants. An indirect effect was also found since exposure to the pollutants at lower trophic levels showed carry over effects on the diversity and abundance of the microbiome on higher trophic levels, even though the organisms at these levels where not directly exposed to the pollutants. Moreover, the exposure to deltamethrin on the damselflies negatively affected their survival rate in the presence of the dragonfly predator, but no such effects were found on damselflies fed with daphnids that had been exposed to microplastics. Conclusions Our study highlights the importance of evaluating ecotoxicological effects at the community level. Importantly, the indirect exposure to microplastics and pesticides through diet can potentially have bottom-up effects on the trophic webs.
... Pesticides can lead to endocrine, hormonal, thyroid, and placental disruption in pregnancy (Mustieles et al., 2017;Silvia et al., 2020;Chevrier et al., 2008;Milczarek et al., 2016;Cecchi et al., 2021) and to thyroid disruption in neonates (Sun et al., 2022). Pesticides can also influence glucose metabolism (Debost-Legrand et al., 2016), immune regulation (Neta et al., 2011;Tyagi et al., 2016), and the bacterial composition of the gut microbiome (Yuan et al., 2019) as well as contribute to environmental enteric dysfunction (EED), a subclinical condition resulting in increased gut permeability and impaired nutrient absorption (Mapesa et al., 2016). ...
... Considerable evidence shows that several mechanisms underlie the associations between pesticide exposure and child growth, including endocrine, hormonal, thyroid, and placental disruption in pregnancy (Mustieles et al., 2017;Silvia et al., 2020;Chevrier et al., 2008;Milczarek et al., 2016;Cecchi et al., 2021), thyroid disruption in the neonatal period (Sun et al., 2022), glucose metabolism disruption (Debost- Legrand et al., 2016), immune dysregulation (Neta et al., 2011;Tyagi et al., 2016), disruption of the gut microbiome (Yuan et al., 2019), and increased gut permeability and impaired nutrient absorption (Mapesa et al., 2016). Despite this considerable literature, empirical evidence on the precise mechanisms through which pesticides influence child growth in LMICs is lacking. ...
Article
Full-text available
Background In low- and middle-income countries (LMICs), pesticides are widely used in agricultural and residential settings. Little is known about how pesticides affect child growth. Objectives To systematically review and synthesise the evidence on the associations between pesticide exposure and adverse birth outcomes and/or impaired postnatal growth in children up to 5 years of age in LMICs. Methods We searched 10 databases from inception through November 2021. We included cohort and cross-sectional studies investigating associations between self-reported or measured prenatal or postnatal pesticide exposure and child growth (postnatal child linear/ponderal growth, and/or birth outcomes). Two researchers screened studies, extracted data, and assessed certainty using GRADE. The protocol was preregistered with PROSPERO (CRD42021292919). Results Of 939 records retrieved, 31 studies met inclusion criteria (11 cohort, 20 cross-sectional). All studies assessed prenatal exposure. Twenty-four studies reported on birth weight. Four found positive associations with organochlorines (0.01–0.25 standardised mean difference (SMD)) and two found negative associations (−0.009 SMD to −55 g). Negative associations with organophosphates (−170 g, n = 1) and pyrethroids (−97 to −233 g, n = 2) were also documented. Two (out of 15) studies reporting on birth length found positive associations with organochlorines (0.21–0.25 SMD) and one found negative associations (−0.25 to −0.32 SMD). Organophosphate exposure was negatively associated with birth length (−0.37 cm, n = 1). Organophosphate exposure was also associated with higher risk/prevalence of low birth weight (2 out of nine studies) and preterm birth (2 out of six studies). Certainty of the evidence was “very low” for all outcomes. Conclusion The limited literature from LMICs shows inconclusive associations between prenatal pesticide exposure, child growth, and birth outcomes. Studies with accurate quantitative data on exposure to commonly used pesticides in LMICs using consistent methodologies in comparable populations are needed to better understand how pesticides influence child growth.
... Furthermore, the gut microbiota promotes high fat diet-induced the in ammation of adipose tissue and increased the expression levels of genes responsible for fatty acid uptake in an FXRdependent manner [39]. In particular, several studies have reported that pesticide exposure can disrupt the gut microbiota of the host [41,42]. Among them, few studies have suggested that the gut microbiota plays an important role in the pesticides' effects on host health [4,43]. ...
... The emerging exploration of the association between pesticides and the host's gut microbiota has completely changed the traditional understanding of pesticide-induced health effects of the host [41,42]. ...
Preprint
Full-text available
Background: The most commonly used organochlorine pesticide nowadays, chlorothalonil (CHI), is ubiquitous in a natural environment and poses many adverse effects to organisms. Unfortunately, the toxicity mechanisms of CHI have not been clarified yet. Results: This study found that the CHI based on acceptable daily intake (ADI) level could induce metabolic syndrome (MetS) in mice, including obesity, hepatic steatosis, dyslipidemia, and insulin resistance. In addition, exposure to reglementary-dose CHI could induce an imbalance in the gut microbiota of mice, resulting in a significant increase in the ratio of Firmicutes to Bacteroidetes. Furthermore, the results of the antibiotic treatment and gut microbiota transplantation experiments showed that the reglementary-dose CHI could induce MetS in mice in a gut microbiota-dependent manner. Based on the results of targeted metabolomics and gene expression analysis, the reglementary-dose CHI could disturb the serum metabolism of bile acids (BAs) in mice, causing the inhibition of the signal response of BAs receptor farnesol X receptor (FXR) and leading to glycolipid metabolism disorders in liver tissue and epididymal white adipose tissue (epiWAT) of mice. The administration of FXR agonist GW4064 and CDCA could significantly improve the reglementary-dose CHI-induced MetS in mice. Conclusions: In conclusion, the reglementary-dose CHI was found to induce MetS in mice by regulating the gut microbiota and BAs metabolism via the FXR signaling pathway. This study provides evidence linking the gut microbiota and pesticides exposure with the progression of MetS, demonstrating the key role of gut microbiota in the toxic effects of pesticides.
... Ahmad et al. (2018) has indicated that the commercial chicken feed and chicken meat contained toxicity of roxarsone, melamine, and pesticides by quantitative and qualitative assessment of additives present in broiler chicken feed and meat. While the host gastrointestinal tract (GIT) functions to digest and absorb nutrients from various feeds, hence the GIT and gut microbiota are likely to be exposed to the pesticides (Yuan et al., 2019). The liver and kidneys are the target organs of some fungicides, which has high relevance with potential hepatotoxic and nephrotoxic effects (Hamdi et al., 2019). ...
... A growing number of studies have indicated that the composition and diversity of the host gut microbiota are readily affected by various types of environmental pollutants including food chemicals and pesticides, suggesting that the role of gut microbiota is getting more and more attention in the study of the pesticide toxicity to non-target organisms (Jin et al., 2017Defois et al., 2018). Yuan et al. (2019) concluded that the correlation between gut microbiota of mammals or zebrafish and health in relation to multiple effects of fungicides and result in physiological disorders of the host. Furthermore, the liver, an important detoxification organ, is the target organ of some fungicides, and it is also the main site for hepatic lipid metabolism, hence the change of liver function is bound to affect the lipid metabolism of host (Jin et al., 2015;Hamdi et al., 2019). ...
Article
Fungicide thiram, a representative dithiocarbamate pesticide can cause potential health hazards to humans and animal health due to the residues in various agricultural products. However, the effects of thiram on lipid metabolism by perturbing gut microbiota of chickens are not clear. Our study was aimed to explore the protective of polysaccharide extracted from Morinda officinalis (MOP) on acute thiram-exposed chickens, and to analyze the association between alteration of gut microbiota and lipid metabolism. Three hundred chicks are fed with a normal diet, thiram-treated diet (100 mg/kg), and a thiram-treated diet supplemented with 250, 500, or 1000 mg/kg MOP was used in this study, respectively. The results showed that thiram exposure prominently elevated liver index, changed liver function by histopathological examination and serum biochemistry diagnoses, and increased blood lipid parameters. Meanwhile, the expression level of some key genes in hepatic lipid metabolism dysregulated significantly in the thiram-exposed chickens. Furthermore, 16S rRNA gene sequencing indicated that thiram exposure can significantly alter the richness, diversity, and composition of the broiler fecal micro-biota, and the relative abundance of Firmicutes and Proteobacteria was also affected at the phylum level. In addition, some microbial populations including Lactobacillus, Ruminococcus, Oscillospira, Blautia, and Butyr-icicoccus significantly decreased at the genus level, whereas the Klebsiella was opposite. Correlation analysis further revealed a significant association between microorganisms and lipid metabolism-related parameters. Optimistically, 500 mg/kg MOP can alleviate the damage of thiram in the gut and liver. Together, these data suggest that thiram exposure causes the imbalance of the gut microbiota and hepatic lipid metabolism disorder in chickens.
... Furthermore, the microbiota induced the in ammation of adipose tissue and increased the expression levels of genes responsible for fatty acid uptake in an FXR-dependent manner [34]. In particular, several studies have reported that pesticide exposure can disrupt the gut microbiota of the host [36,37]. Among them, few studies have suggested that the gut microbiota plays an important role in the pesticides' effects on host health [4,38]. ...
... The emerging exploration of the association between pesticides and the host's gut microbiota has completely changed the traditional understanding of pesticide-induced health effects of the host [36,37]. Several studies have proved the close association between gut microbiota and MetS [40][41][42]. ...
Preprint
Full-text available
Background:The most commonly used organochlorine pesticide, chlorothalonil (CHI), is ubiquitous in a natural environment and poses many adverse effects to organisms. Unfortunately, the toxicity mechanisms of CHI have not been clarified yet. Results: This study found that the low-dose CHI based on acceptable daily intake (ADI) level could induce metabolic syndrome (MetS) in mice, including obesity, hepatic steatosis, dyslipidemia, and insulin resistance. In addition, exposure to low-dose CHI could induce an imbalance in the gut microbiota of mice, resulting in a significant increase in the ratio of Firmicutes to Bacteroidetes. Furthermore, the results of the antibiotic treatment and gut microbiota transplantation experiments showed that the low-dose CHI could induce MetS in mice in a gut microbiota-dependent manner. Based on the results of targeted metabolomics and gene expression analysis, the low-dose CHI could disturb the serum metabolism of bile acids (BAs) in mice, causing the inhibition of the signal response of BAs receptor farnesol X receptor (FXR) and leading to glycolipid metabolism disorders in liver tissue and epididymal white adipose tissue (epiWAT) of mice. The administration of FXR agonist GW4064 and CDCA could significantly improve the low-dose CHI-induced MetS in mice. Conclusions: In conclusion, the low-dose CHI was found to induce MetS in mice by regulating the gut microbiota and BAs metabolism via the FXR signaling pathway. This study provides evidence linking the gut microbiota and pesticides exposure with the progression of MetS, demonstrating the key role of gut microbiota in the toxic effects of pesticides.
... The important aspects of the fate of pesticides in the rhizosphere and animal guts to be considered are their interference with metabolic processes and genetic exchanges (i.e., HGT (horizontal gene transfer) events) through the associated microbiomes of the hosts. The effects of pesticides on the gut microbiomes and human health are being understood (Montgomery et al. (2008); Yuan et al., 2019;Meng et al., 2020); however, the commonalities among the microbiomes of rhizosphere and insect gut remain unrecognized. Although there exist close linkages between microbiomes of soil and human gut, the impact of pesticide interactions with the microbiomes of plant rhizosphere and animal guts has not been elucidated so far. ...
... But the 'dysbiotic' gut microbiota can induce many autoimmune conditions in human diseases such as type 1 diabetes, rheumatoid arthritis, and inflammatory bowel diseases. Pesticide exposure to humans can cause obesity, endocrine disruption, and other immunity-related disorders with alterations in the metabolism due to the gut microbiota perturbation (Montgomery et al., 2003;Yuan et al., 2019;Kaur et al., 2020;Meng et al., 2020). The associations between a specific pesticide and human metabolic disorders including cancer are difficult to detect and attribute but are generally consistent for high and prolonged exposures (for select pesticide-induced diseases of human digestive system, see Table 3). ...
Article
Pesticides are becoming a significant transnational pollutant in agricultural production environments. This review presents the interconnectedness and interaction effects of pesticides with the microbiomes in the environments of plant rhizosphere and animal (limited to insect and human) guts. The metabolic growth and functions of rhizosphere microbiomes are altered by complex mechanisms involving redox reactions and preferential substrate utilization. The rhizospheres of crop plants with the assemblies of microbiota and other biotic components are sensitive to the deliberate introduction of pesticides. Pesticides become one of the major drivers for the metabolic processes, which rely on the evolutionary mechanisms, including the genetic exchange events within the rhizosphere microbiomes. Pesticides, even at the below detection levels, in the rhizosphere enable the plant uptake which can be up to 1% of the dose applied and trophic transfers involving the animal gut environments. To overcome the metabolic constraints due to the nutrient-poor plant diets contaminated with pesticides, insects gain the resistance traits, mainly due to the pesticide-degrading members of the gut microbiomes. Such evolved microbiome members and their genes can increase their spread of resistance in the environment. Like the insect gut microbiomes, the human gut microbiomes get modulated by the pesticide-laden plant foods, leading to dysbiosis. The confounding effects of pesticides on the gut microbiomes which include mutational and genetic exchange events can upsurge many health disorders. The evolutionary and microbiome perspectives on the rhizosphere and animal guts as the hotspots of metabolic and horizontal gene transfer (HGT) events need careful considerations to mitigate the risks and health hazards due to extensive and intensive application of synthetic chemical pesticides in the modern agriculture.
... By taking them as a low toxicity chemical, the potential effects of fungicides on animal and human health have often been ignored. However, with the development of analytical techniques, data on the toxicity of fungicides in different experimental models has drastically increased [10][11][12]. ...
Article
Full-text available
Carbendazim (CBZ) as a fungicide is widely used to control fungal diseases in agriculture, veterinary medicine, and forestry. In this study, molecularly imprinted nano-size polymer was synthesized and then combined with multiwalled carbon nanotubes to be used as modifiers for carbon paste electrode to detect carbendazim in water, fruit, agricultural wastewater, and urine samples by using the square-wave technique. Some common ions and pesticides were investigated as interferences in analyte, to study the sensitivity and selectivity of the modified carbon paste electrode for carbendazim. The combination of molecular imprinted polymer and multiwalled carbon nanotubes showed a significant increase in peak current in electrocatalytic activity on electrochemical detection of the carbendazim. The linear range of 1 × 10-10 to 5 × 10-8 molL-1 was investigated. The lower detection limit was determined to be 0.2 × 10-10 molL-1, and the relative standard deviation for the target molecule analysis was 2.07%. The result reveals that the modified carbon paste sensor with Multi walled Carbon Nanotubes (MWCNTs) and Molecular Imprinted Polymer (MIPs) can be used easily, without preparation steps that have high selectivity and sensitivity to determine carbendazim in water, fruit, agricultural wastewater, and urine samples.
... Then, livestock and fish accumulate more toxic substances in the body from these grains, grass, and environment. These toxic substances will probably pass to humans through food chains, disrupt human gut microbiota, and induce neurotoxicity and brain impairment through microbiota-gut-brain axis (43,92,94,(102)(103)(104). ...
Article
Full-text available
Introduction The highly processed western diet is substituting the low-processed traditional diet in the last decades globally. Increasing research found that a diet with poor quality such as western diet disrupts gut microbiota and increases the susceptibility to various neurological and mental disorders, while a balanced diet regulates gut microbiota and prevents and alleviates the neurological and mental disorders. Yet, there is limited research on the association between the disease burden expanding of neurological and mental disorders with a dietary transition. Methods We compared the disability-adjusted life-years (DALYs) trend by age for neurological and mental disorders in China, in the United States of America (USA), and across the world from 1990 to 2019, evaluated the dietary transition in the past 60 years, and analyzed the association between the burden trend of the two disorders with the changes in diet composition and food production. Results We identified an age-related upward pattern in disease burden in China. Compared with the USA and the world, the Chinese neurological and mental disorders DALY percent was least in the generation over 75 but rapidly increased in younger generations and surpassed the USA and/or the world in the last decades. The age-related upward pattern in Chinese disease burdens had not only shown in the presence of cardiovascular diseases, neoplasms, and diabetes mellitus but also appeared in the presence of depressive disorders, Parkinson’s disease, Alzheimer’s disease and other dementias, schizophrenia, headache disorders, anxiety disorders, conduct disorders, autism spectrum disorders, and eating disorders, successively. Additionally, the upward trend was associated with the dramatic dietary transition including a reduction in dietary quality and food production sustainability, during which the younger generation is more affected than the older. Following the increase in total calorie intake, alcohol intake, ratios of animal to vegetal foods, and poultry meat to pulses, the burdens of the above diseases continuously rose. Then, following the rise of the ratios of meat to pulses, eggs to pulses, and pork to pulses, the usage of fertilizers, the farming density of pigs, and the burdens of the above disease except diabetes mellitus were also ever-increasing. Even the usage of pesticides was positively correlated with the burdens of Parkinson’s disease, schizophrenia, cardiovascular diseases, and neoplasms. Contrary to China, the corresponding burdens of the USA trended to reduce with the improvements in diet quality and food production sustainability. Discussion Our results suggest that improving diet quality and food production sustainability might be a promising way to stop the expanding burdens of neurological and mental disorders.
... According to previous published studies, pesticides could induce gut inflammation and improve intestinal permeability, which allows chemical pollutants and pathogenic bacteria to cross the intestinal barrier and enter the blood, thereby leading to systemic inflammation and multi-organ injury (Wang et al., 2021a,b). Gut microbiota has been indicated in playing a role in pesticide-induced health issues (Meng et al., 2020;Yuan et al., 2019). For example, fungicide (Prothioconazole) promotes liver damage by impacting gut microbiota and intestinal barrier function (Meng et al., 2021). ...
Article
Pesticide thiram is widely used in agriculture and has been demonstrated to cause tibial dyschondroplasia (TD) in birds. However, the underlying mechanism remains unclear. This work used multi omics analysis to evaluate the molecular pathways of TD in broilers that were exposed to low level of thiram. Integrative analysis of transcriptomic, proteomic, and metabolomic revealed thiram activity in enhancing pathological ECM remodeling via attenuating the glycolysis pathway and activating the hexosamine and glucuronic acid pathways. Intriguingly, we found hyperglycemia as a crucial factor for ECM overproduction, which resulted in the development of TD. We further demonstrated that high glucose levels are caused by islet secretion dysfunction in thiram-treated broilers. A combination of factors, including lipid disorder, low-grade inflammation, and gut flora disturbance, might contribute to the dysregulation of insulin secretion. The current work revealed the underlying toxicological mechanisms of thiram-induced tibial dyschondroplasia through blood glucose disorder via the gutpancreas axis in chickens for the first time, which makes it easier to figure out the health risks of pesticides for worldwide policy decisions.
... Moreover, chemicals triggers may impair the functions of GI epithelial cells by upregulation of TLR-4, which can activate inflammatory paths with cytokine storms and production of harmful ROS (Yuan et al., 2019a). Indeed, Gao et al. recently used mice to explore the effects of lead on the microbiome via both whole-genome metagenomics and metabolomics sequencing, indicating that lead exposure can affect the uniformity of the microbiome and of several associated biochemical pathways including oxidative stress and detoxification functions (Assefa & Köhler, 2020;Gao et al., 2017) Due to inflammation activation, the lipo-polysaccharide (LPS), a gram-negative bacterial endotoxin, can be then increasingly released into the gut and act on the TLR-4 of innate immune cells (Gillois et al., 2018). ...
Article
The explosion of microbiome research over the past decade has shed light on the various ways that external factors interact with the human microbiome to drive health and disease. Each individual is exposed to more than 300 environmental chemicals every day. Accumulating evidence indicates that the microbiome is involved in the early response to environmental toxicants and biologically mediates their adverse effects on human health. However, few review articles to date provided a comprehensive framework for research and translation of the role of the gut microbiome in environmental health science. This review summarizes current evidence on environmental compounds and their effect on the gut microbiome, discusses the involved compound metabolic pathways, and covers environmental pollution-induced gut microbiota disorders and their long-term outcomes on host health. We conclude that the gut microbiota may crucially mediate and modify the disease-causing effects of environmental chemicals. Consequently, gut microbiota needs to be further studied to assess the complete toxicity of environmental exposures. Future research in this field is required to delineate the key interactions between intestinal microbiota and environmental pollutants and further to elucidate the long-term human health effects.
... The primary way of transformation of pesticides in the general population is the consumption of food commodities that might be polluted with toxic residues of pesticides (Nagy et al., 2020). However, their residues can ultimately be inserted into animals' digestive tracts via various pathways and affect their physical conditions (Altun et al., 2017;Yuan et al., 2019). Recently, Nerozzi et al. (2020) investigated the effects of glyphosate and its most famous formulation Roundup, on animal health and reproductive functions. ...
Article
Full-text available
Synthetic pesticides are extensively and injudiciously applied to control agriculture and household pests worldwide. Due to their high use, their toxic residues have enormously increased in the agroecosystem in the past several years. They have caused many severe threats to non-target organisms, including humans. Therefore, the complete removal of toxic compounds is gaining wide attention to protect the ecosystem and the diversity of living organisms. Several methods, such as physical, chemical and biological, are applied to degrade compounds, but as compared to other methods, biological methods are considered more efficient, fast, eco-friendly and less expensive. In particular, employing microbial species and their purified enzymes makes the degradation of toxic pollutants more accessible and converts them into non-toxic products by several metabolic pathways. The digestive tract of insects is usually known as a superior organ that provides a nutrient-rich environment to hundreds of microbial species that perform a pivotal role in various physiological and ecological functions. There is a direct relationship between pesticides and insect pests: pesticides reduce the growth of insect species and alter the phyla located in the gut microbiome. In comparison, the insect gut microbiota tries to degrade toxic compounds by changing their toxicity, increasing the production and regulation of a diverse range of enzymes. These enzymes breakdown into their derivatives, and microbial species utilize them as a sole source of carbon, sulfur and energy. The resistance of pesticides (carbamates, pyrethroids, organophosphates, organochlorines, and neonicotinoids) in insect species is developed by metabolic mechanisms, regulation of enzymes and the expression of various microbial detoxifying genes in insect guts. This review summarizes the toxic effects of agrochemicals on humans, animals, birds and beneficial arthropods. It explores the preferential role of insect gut microbial species in the degradation process and the resistance mechanism of several pesticides in insect species. Additionally, various metabolic pathways have been systematically discussed to better understand the degradation of xenobiotics by insect gut microbial species.
... The gastrointestinal tract, as an indispensable part of the human body also susceptible to pesticides, the causality between the gut microbiota and pesticide induced-toxicity been gaining increasing attention recently (Yuan et al., 2019). The gut microenvironment facilitates the growth of divisions bacteria, different gut microbiota performs their functions in different landscapes in the human body such as producing various metabolites, BAs are one of them (Al Bander et al., 2020). ...
Article
The triazole fungicide prothioconazole (PTC) can cause adverse effects in animals, and its main metabolite prothioconazole-desthio (PTC-d) is even much more harmful. However, the toxic effects of PTC and PTC-d on the liver-gut axis of mice are still unknown. In the present experiment, we found that oral exposure to PTC and PTC-d increased total bile acids (TBAs) levels in the serum, liver, and feces. Correspondingly, the transcription of genes involved in bile acids (BAs) disposition was significantly influenced by PTC or PTC-d exposure. Furthermore, the BAs composition of serum BAs was analyzed by LC-MS, and the results indicated that PTC and PTC-d exposure changed the BAs composition, lowered the ratio of conjugated/unconjugated BAs, elevated the ratio of CA/b-MCA, and enhanced the hydrophobicity of BAs pool. 16s RNA gene sequencing of the DNA from colonic contents uncovered that PTC and PTC-d exposure altered the relative abundance and constitution of intestinal microbiota, increasing the relative level of Lactobacillus with bile salt hydrolase (BSH) activity. Furthermore, PTC and PTC-d exposure impaired the gut barrier function, causing an increase in mucus secretion. In particular, the effects of PTC-d on some endpoints in the BAs metabolism and gut barrier function had been proven to be more significant than the parent compound PTC. All these findings draw attention to the health risk of PTC and PTC-d exposure in regulating BAs metabolism, which might lead to some metabolic disorders and occur of related diseases in animals.
... The intestine not only is responsible for the digestion and absorption of nutrients but also is the largest immune organ that is closely related to the health of animals (14,15). It plays a crucial role in resisting the invasion of pathogenic bacteria and the entry of xenobiotics (16). ...
Article
Full-text available
Hexavalent chromium [Cr(VI)] is a dangerous heavy metal which can impair the gastrointestinal system in various species; however, the processes behind Cr(VI)-induced intestinal barrier damage are unknown. Forty-eight healthy 1-day-old ducks were stochastically assigned to four groups and fed a basal ration containing various Cr(VI) dosages for 49 days. Results of the study suggested that Cr(VI) exposure could significantly increase the content of Cr(VI) in the jejunum, increase the level of diamine oxidase (DAO) in serum, affect the production performance, cause histological abnormalities (shortening of the intestinal villi, deepening of the crypt depth, reduction and fragmentation of microvilli) and significantly reduced the mRNA levels of intestinal barrier-related genes (ZO-1, occludin, claudin-1, and MUC2) and protein levels of ZO-1, occludin, cand laudin-1, resulting in intestinal barrier damage. Furthermore, Cr(VI) intake could increase the contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-18 (IL-18) but decrease the activities of total superoxide dismutase (T-SOD), catalase (CAT), and glutathione reductase (GR), as well as up-regulate the mRNA levels of TLR4, MyD88, NF-κB, TNFα, IL-6, NLRP3, caspase-1, ASC, IL-1β, and IL-18 and protein levels of TLR4, MyD88, NF-κB, NLRP3, caspase-1, ASC, IL-1β, and IL-18 in the jejunum. In conclusion, Cr(VI) could cause intestinal oxidative damage and inflammation in duck jejunum by activating the NF-κB signaling pathway and the NLRP3 inflammasome.
... Pesticide pollutions have common health hazards over the last several decades because of the widespread in the world (Yuan et al. 2019). Most countries have banned organophosphate and organochlorine pesticides due to their high toxicity and bioaccumulation in non-target animals. ...
Chapter
Aquaculture is one of the fastest-growing industries in the world, and it primarily helps to boost global production. The possibility of cultured fish demonstrating their genetic capacity for growth and reproduction major crucial factor determined by nutrition. Because of the limitation on the use of various antibiotics, as well as their cost-effectiveness, natural feed additives are an external source of aquaculture output. The enhancement in cost scarcity of supplies of fish feed has necessitated more study into replacements. Many researchers have recently demonstrated the benefits of medicinal herbs as feed additives. Even consumers are concerned about using antibiotics instead of natural feed additives to increase aquaculture quality. The determination of feed additives is to suppress pathogenic bacteria, improve growth, stimulate the immune system, and assure water purity. Essential oils, essential fatty acids, probiotics and prebiotics, synbiotics, and exogenous enzymes were all used in several types of feed additives. These additives were praised for their unique medical capabilities as well as their eco-friendly digestive system metabolisms. However, utilizing crops in feeds increases the risk of fungus and mycotoxins contamination, as well as the incidence of mycotoxicosis in fish. Because mycotoxicosis causes decreased bodyweight, growth impairment, and greater rates of disease and mortality in fish, this could reduce aquaculture productivity. This chapter highlights the cumulative research findings on various feed additives, and aquaculture production quality and mycotoxins impair the animal immune systems.
... Widely used pesticides are present in our daily life [1]. The harm of low concentration pesticide residues to humans and animals can be ignored, but with the improvement of analytical methods, more and more experiments prove that pesticide residues in the environment exceed the standard [2,3]. Pesticide residue hazards have become a growing concern. ...
Article
Full-text available
Atrazine (ATZ) is a herbicide used in agricultural production and has been detected in surface water due to its widespread use worldwide. This may pose a threat to the health of aquatic animals. To explore the ATZ−induced hepatic metabolism disorder, male zebrafish were exposed to 300 and 1000 μg/L ATZ for 21 days, respectively. The results revealed that ATZ exposure significantly reduced hepatic triglyceride (TG) levels, while significantly (p < 0.05) increased pyruvate (PYR) and total cholesterol (TC) levels. In addition, the liver sample from the 1000 μg/L ATZ−treated group was used for GC/MS metabolomic analysis. The principal component analysis (PCA) model showed significant separation of the 1000 μg/L ATZ group from the control group, indicating that ATZ exposure altered hepatic metabolism in male adult zebrafish. A total of 29 significantly (p < 0.05) different metabolites were observed and identified in the ATZ−treated group. Moreover, the most disturbed pathways by ATZ were the arginine and proline metabolic pathways, followed by the glutathione metabolic pathway. Three and two metabolites were significantly altered in the arginine and proline metabolic pathways and glutathione metabolic pathway, respectively. Based on these results, we suggested that ATZ was capable of altering liver metabolism in zebrafish and that its ecological risk to aquatic organisms cannot be ignored.
... Combining both in utero and after-birth exposures, NITs and their HGM is exposed to multiple classes of chemicals of dietary and environmental origin (Figure 1). Recent reviews covering interactions between the HGM and xenobiotics are available for mycotoxins [52], pesticide residues [26], drugs [53], herbal medicines [50], heavy metals, food additives, and antibiotics [54]. However, data from Africa are scarce and are thus vastly under-reported in these reviews, and there are several outstanding knowledge gaps that need to be addressed [55]. ...
Article
Full-text available
The gut microbiome of neonates, infants, and toddlers (NITs) is very dynamic, and only begins to stabilize towards the third year of life. Within this period, exposure to xenobiotics may perturb the gut environment, thereby driving or contributing to microbial dysbiosis, which may negatively impact health into adulthood. Despite exposure of NITs globally, but especially in Africa, to copious amounts and types of xenobiotics – such as mycotoxins, pesticide residues, and heavy metals – little is known about their influence on the early-life microbiome or their effects on acute or long-term health. Within the African context, the influence of fermented foods, herbal mixtures, and the delivery environment on the early-life microbiome are often neglected, despite being potentially important factors that influence the microbiome. Consequently, data on in-depth understanding of the microbiome–exposome interactions is lacking in African cohorts. Collecting and evaluating such data is important because exposome-induced gut dysbiosis could potentially favor disease progression.
... In recent years, many studies have indicated that environmental pesticides exposure will cause fish intestine barrier damage and intestine microbiota dysbiosis, such as organophosphate and organochlorine pesticides (Hua et al., 2021;Wang et al., 2019), pyrethroid (Yuan et al., 2019), neonicotinoids (Luo et al., 2021), glyphosate (Faria et al., 2021, imazalil (Jin et al., 2017) and carbendazim (Bao et al., 2020). The intestine barrier is a very important line of defense for preventing the exogenous substances, thereby ensuring the intestine health of fish . ...
Article
The indiscriminate use of deltamethrin in agriculture and aquaculture can lead to residues increased in many regions, which poses negative impacts on intestinal health of aquatic organisms. Although the potential toxicity of deltamethrin have recently attracted attention, the comprehensive studies on intestinal injuries after chronic deltamethrin exposure remain poorly understood. Herein, in a 28-day chronic toxicity test, crucian carp expose to different concentrations of deltamethrin (0, 0.3, and 0.6 μg/L) were used as the research object. We found that the morphology changes and increased goblet cells in intestinal tissue, and the extent of tissue injury increased along with the increasing exposure dose of deltamethrin. Additionally, the genes expression of antioxidant activity (Cu/Zn superoxide dismutase (Cu-Zn SOD), glutathione peroxidase 1 (GPX1), and catalase (CAT)), inflammatory response (tumor necrosis factor alpha (TNFα), interferon gamma (IFNγ), and interleukin 1 beta (IL-1β)), and tight junctions (Claudin 12 (CLDN12), and tight junction protein 1 (ZO-1)) dramatically increased. Meanwhile, the apoptosis and autophagy process were triggered through caspase-9 cascade and autophagy related 5 (ATG5)- autophagy related 12 (ATG12) conjugate. Besides, chronic deltamethrin exposure increased the amount of Proteobacteria and Verrucomicrobiota, while decreased Fusobacteriota abundance, resulting in intestinal microbiota function disorders. In summary, our results highlight that chronic exposure to deltamethrin cause serious intestinal toxicity and results in physiological changes and intestinal flora disturbances.
... Potential mechanisms for reduced SCFA-producing bacteria could relate to lifestyle factors including diet, physical activity, and sleep, as previously discussed (Nuzum et al., 2020). Additional mechanisms may include the use of antibiotics (Parada Venegas et al., 2019) or exposure to environmental toxins including pesticides or heavy metals which have been shown to alter the microbiome of animal models (Yuan et al., 2019). Mice exposed to chlorpyrifos had increased markers of inflammation and intestinal permeability, along with reductions in some SCFA metabolites (Zhao et al., 2016). ...
Article
Full-text available
There is continued debate regarding Parkinson’s disease etiology and whether it originates in the brain or begins in the gut. Recently, evidence has been provided for both, with Parkinson’s disease onset presenting as either a “body-first” or “brain-first” progression. Most research indicates those with Parkinson’s disease have an altered gut microbiome compared to controls. However, some studies do not report gut microbiome differences, potentially due to the brain or body-first progression type. Based on the etiology of each proposed progression, individuals with the body-first progression may exhibit altered gut microbiomes, i.e., where short-chain fatty acid producing bacteria are reduced, while the brain-first progression may not. Future microbiome research should consider this hypothesis and investigate whether gut microbiome differences exist between each type of progression. This may further elucidate the impact of the gut microbiome in Parkinson’s disease and show how it may not be homogenous across individuals with Parkinson’s disease.
... Environmental exposures to chemical pollutants can alter host microbial communities through absorption, inhalation, and consumption, eliciting specific physiological responses from the nervous, endocrine, and immune systems (Peisl et al., 2018). For example, exposure to the pesticide chlorpyrifos resulted in a decrease in beneficial bacteria and increases in gut permeability and inflammation in mice (Yuan et al., 2019), as well as inducing obesity and insulin resistance (Liang et al., 2019). Giving these mice a broadspectrum antibiotic affecting their gut microbiota reversed the effects. ...
Article
Sixty years ago, Rachel Carson published her book Silent Spring, which focused the world's attention on the dangers of pesticides. Since that time human impacts on the environment have accelerated and this has included reshaping the chemical landscape. Here we evaluate the severity of exposure of tropical terrestrial mammals to pesticides, pharmaceuticals, plastics, particulate matter associated with forest fires, and nanoparticles. We consider how these environmental contaminants interact with one another, with the endocrine and microbiome systems of mammals, and with other environmental changes to produce a larger negative impact than might initially be expected. Using this background and building on past conservation success, such as mending the ozone layer and decreasing acid rain, we tackle the difficult issue of how to construct meaningful policies and conservation plans that include a consideration of the chemical landscape. We document that policy solutions to improving the chemical landscape are already known and the path of how to construct a healthier planet is discernible.
... www.advancedsciencenews.com www.advnanobiomedres.com and archaea, maintain a symbiotic relationship with the host by producing antimicrobial compounds while also competing for nutrients and colonization spaces in the gut, thereby resisting the invasion of pathogens. [28] The gastrointestinal tract microorganisms also play important roles in the training of gut immunity. To date, characterization of the biological barrier is mainly based on the character and function of bacteria colonizing the gut; however, a growing number of gut fungi, viruses, and archaea are being identified with the rapid development of bioinformation technologies. ...
Article
Full-text available
The intestinal barrier plays a vital role in maintaining the homeostasis of the gut and the organism. Various nanomedicines with advantages in interacting with the intestinal barrier have been developed for disease treatment. Previous studies indicate multiple interactions between these nanomaterials and the intestinal barrier, boosting their applications in promoting the efficiency of oral drug delivery. Recently, numerous elegant nanomedicines have been developed for preventing and treating both intestinal and extraintestinal diseases. Integration of multiple elements with diverse functions into a single type of nanomedicine is beneficial for comprehensive regulation of its interaction with the intestinal barrier and the corresponding treatment efficacy. In this review, the interactions between nanomaterials and the intestinal barrier are discussed following an introduction of the structure and function of the intestinal barrier, with an aim to better understanding the rational design of effective nanomedicines, particularly for oral delivery. Lastly, the applications of oral nanomedicines in treating intestinal barrier dysfunction and relevant diseases, such as inflammatory bowel disease, diabetes, arthritis, and cancer, are highlighted. It is anticipated that this review will stimulate more innovative thinking focused on the intestinal barrier as a critical target for drug delivery and disease treatment. To better understand the rational design of nanomedicines, particularly for oral delivery, the interactions between nanomaterials and the intestinal barrier are discussed, followed by an introduction of oral nanomedicines for treating intestinal barrier dysfunction and relevant diseases. This review stimulates more innovative thinking focused on the intestinal barrier as a critical target for drug delivery and disease treatment.
... Polybrominated diphenyl ethers (PBDEs) are environmentally persistent chemicals widely used as flame retardants [18] that have been shown to alter microbiota [19]. Pesticides have been shown to have important implications for environmental, animal, and human health [20]. Glyphosate and chlorpyrifos exposure occur mainly through diet and drinking water [21]. ...
Article
Full-text available
Chemical risk assessment in the context of the risk analysis framework was initially designed to evaluate the impact of hazardous substances or xenobiotics on human health. As the need of multiple stressors assessment was revealed to be more reliable regarding the occurrence and severity of the adverse effects in the exposed organisms, the cumulative risk assessment started to be the recommended approach. As toxicant mixtures and their “cocktail effects” are considered to be main hazards, the most important exposure for these xenobiotics would be of dietary and environmental origin. In fact, even a more holistic prism should currently be considered. In this sense, the definition of One Health refers to simultaneous actions for improving human, animal, and environmental health through transdisciplinary cooperation. Global policies necessitate going beyond the classical risk assessment for guaranteeing human health through actions and implementation of the One Health approach. In this context, a new perspective is proposed for the integration of microbiome biomarkers and next generation probiotics potentially impacting and modulating not only human health, but plant, animal health, and the environment.
... The effect of pesticides on the host gut microbiota has recently benefited from a growing interest, as the gut constitutes the primary site of interaction with ingested pesticides 28,29 . The honey bee gut harbors a specific bacterial community of low taxonomic complexity dominated by eight to ten bacterial phylotypes [30][31][32][33] , five of which (Gilliamella apicola, Snodgrassella alvi, Bifidobacterium asteroides, Lactobacillus Firm-4 and Lactobacillus Firm-5) represent the core gut microbiota found in every honey bee worker throughout the planet 34 . ...
Article
Full-text available
Recent studies highlighted that exposure to glyphosate can affect specific members of the core gut microbiota of honey bee workers. However, in this study, bees were exposed to relatively high glyphosate concentrations. Here, we chronically exposed newly emerged honey bees to imidacloprid, glyphosate and difenoconazole, individually and in a ternary mixture, at an environmental concentration of 0.1 µg/L. We studied the effects of these exposures on the establishment of the gut microbiota, the physiological status, the longevity, and food consumption of the host. The core bacterial species were not affected by the exposure to the three pesticides. Negative effects were observed but they were restricted to few transient non-core bacterial species. However, in the absence of the core microbiota, the pesticides induced physiological disruption by directly altering the detoxification system, the antioxidant defenses, and the metabolism of the host. Our study indicates that even mild exposure to pesticides can directly alter the physiological homeostasis of newly emerged honey bees and particularly if the individuals exhibit a dysbiosis (i.e. mostly lack the core microbiota). This highlights the importance of an early establishment of a healthy gut bacterial community to strengthen the natural defenses of the honey bee against xenobiotic stressors.
... The impact of these chemical substances on this microbiome has been broadly documented (Maier et al., 2018;Chiu et al., 2020;Roca-Saavedra et al., 2018;Laudisi, Stolfi, and Monteleone, 2019). Pesticide food residues constitute one of the main groups of chemicals with which the intestinal microbiota is regularly confronted (Yuan et al., 2019;Roman et al., 2019;Utembe and Kamng'ona 2021;Meng et al., 2020). The organophosphorus pesticide chlorpyrifos (CPF: O, O-diethyl-O-(3,5, 6-trichloro-2-pyridinyl) phosphorothioate) is a good example of this group. ...
Article
The intestinal microbiota has a key role in human health via the interaction with the somatic and immune cells in the digestive tract environment. Food, through matrix effect, nutrient and non-nutrient molecules, is a key regulator of microbiota diversity. As a food contaminant, the pesticide chlorpyrifos (CPF) has an effect on the composition of the intestinal microbiota and induces perturbation of microbiota. Prebiotics (and notably inulin) are known for their ability to promote an equilibrium of the microbiota that favours saccharolytic bacteria. The SHIME® dynamic in vitro model of the human intestine was exposed to CPF and inulin concomitantly for 30 days, in order to assess variations in both the bacterial populations and their metabolites. Various analyses of the microbiota (notably temporal temperature gradient gel electrophoresis) revealed a protective effect of the prebiotic through inhibition of the enterobacterial (E. coli) population. Bifidobacteria were only temporarily inhibited at D15 and recovered at D30. Although other potentially beneficial populations (lactobacilli) were not greatly modified, their activity and that of the saccharolytic bacteria in general were highlighted by an increase in levels of short-chain fatty acids and more specifically butyrate. Given the known role of host-microbiota communication, CPF's impact on the body's homeostasis remains to be determined.
... The median lethal doses of pesticides for honey bees are generally lower than those for bumble bees and higher than those for stingless bees (perhaps owing to the size differences among these taxa, since doses are often measured in μg bee -1 ), although stingless bees show an immense range of interspecific variation (Arena and Sgolastra 2014; Sanchez-Bayo and Goka 2014). One of the ways that pesticides disturb gut microbiotas is by impairing host health to the point that the host is unable to properly regulate its gut microbiota, leading to dysbiosis (Box 1; Fig. 2) (Yuan et al. 2019). If social corbiculate bee species differ in their pesticide sensitivities, the doses of pesticides and durations of exposure that cause gut microbiota dysbiosis via a decline in host health likely vary as well. ...
Article
Social bee gut microbiotas play key roles in host health and performance. Worryingly, a growing body of literature shows that pesticide exposure can disturb these microbiotas. Most studies examine changes in taxonomic composition in Western honey bee (Apis mellifera) gut microbiotas caused by insecticide exposure. Core bee gut microbiota taxa shift in abundance after exposure but are rarely eliminated, with declines in Bifidobacteriales and Lactobacillus near melliventris abundance being the most common shifts. Pesticide concentration, exposure duration, season and concurrent stressors all influence whether and how bee gut microbiotas are disturbed. Also, the mechanism of disturbance-i.e. whether a pesticide directly affects microbial growth or indirectly affects the microbiota by altering host health-likely affects disturbance consistency. Despite growing interest in this topic, important questions remain unanswered. Specifically, metabolic shifts in bee gut microbiotas remain largely uninvestigated, as do effects of pesticide-disturbed gut microbiotas on bee host performance. Furthermore, few bee species have been studied other than A. mellifera, and few herbicides and fungicides have been examined. We call for these knowledge gaps to be addressed so that we may obtain a comprehensive picture of how pesticides alter bee gut microbiotas, and of the functional consequences of these changes.
... Therefore, future studies investigating the changes in the workers' microbiota according to different occupational factors and the seasonal variability are needed to better understand the interconnections in this relationship. Numerous studies confirm the modifications that pesticides can induce at the microbiota level and particularly involve the gut-brain axis [65,100,101]. Several studies have proven that there is a strong connection between the gut microbiota and the brain and called this connection "the gut-brain axis". ...
Article
Full-text available
The characterization of human microbiota and the impact of its modifications on the health of individuals represent a current topic of great interest for the world scientific community. Scientific evidence is emerging regarding the role that microbiota has in the onset of important chronic illnesses. Since individuals spend most of their life at work, occupational exposures may have an impact on the organism’s microbiota. The purpose of this review is to explore the influence that different occupational exposures have on human microbiota in order to set a new basis for workers’ health protection and disease prevention. The literature search was performed in PubMed, Cochrane, and Scopus. A total of 5818 references emerged from the online search, and 31 articles were included in the systematic review (26 original articles and 5 reviews). Exposure to biological agents (in particular direct contact with animals) was the most occupational risk factor studied, and it was found involved in modifications of the microbiota of workers. Changes in microbiota were also found in workers exposed to chemical agents or subjected to work-related stress and altered dietary habits caused by specific microclimate characteristics or long trips. Two studies evaluated the role of microbiota changes on the development of occupational lung diseases. Occupational factors can interface with the biological rhythms of the bacteria of the microbiota and can contribute to its modifications and to the possible development of diseases. Future studies are needed to better understand the role of the microbiota and its connection with occupational exposure to promote projects for the prevention and protection of global health.
... Our previous studies suggested that xenobiotics, especially environmental pollutants, including antibiotics, microplastic and fungicides, caused gut microbiota disorder and impact the intestinal barrier [14,27,28]. The intestinal mucus layer is one crucial part of the gut barrier to preventing foreign invasion [16]. ...
Article
Full-text available
Difenoconazole (DIF) is a widely separated triazole fungicide in many countries. The excessive usage of DIF increases the high volume of residues in agriculture production and water bodies. Some previous studies demonstrated the toxic effects of DIF on non-target animals, however, there were still some gaps in the knowledge of the potential hazards of DIF to mammals and human health. Herein, 7-week-old male mice were exposed to 30 and 100 mg/kg/day DIF for 14 and 56 days. We observed that 56 days of DIF exposure decreased the colonic mucus expression of alcin blue-periodic acid-schiff (AB-PAS) stain and the immunochemical stain of muc2 protein. The transcript levels of mucin protein (muc1, muc2 and muc3) decreased significantly in the gut of mice followed 56 days of 100 mg/kg/day DIF exposure. In addition, the gut microbiota composition was also affected after 14 or 56 days of DIF exposure. Although the mucus expression after 14 days of DIF exposure only decreased slightly, the gut microbiota composition compared with the control group was changed significantly. Moreover, the DIF-30 and DIF-100 caused respectively different changes on the gut microbiota. The relative abundance of Bacteroidetes decreased significantly after 14 days and 56 days of DIF exposure. After 14 days of DIF exposure, there were 35 and 18 differential genera in the DIF-30 and DIF-100 group, respectively. There were 25 and 32 differential genera in the DIF-30 and DIF-100 group after 56 days of exposure, respectively. Meanwhile, the alpha diversity indexes, including observed species, Shannon, Simpson, Chao1 and ACE, in gut microbiota decreased significantly after 56 days of DIF exposure. Interestingly, the relative abundance of Akkermansia increased significantly after 56 days of 100 mg/kg/d DIF exposure. Although Akkermansia was considered as one probiotic, the phenomenon of dramatic Akkermansia increase with the decrease in gut microbiota diversity needed further discussion. These results provided some new insights on how DIF exposure impacts the mucus barrier and induces gut microbiota dysbiosis.
... Gene expression in these microorganisms increased in the presence of pesticides [31]. Studies have shown that pesticides can interact with gut microbiota, affecting the receptor sites of different tissues and organs, destroying the intestinal mucosa and cells that lead to pathological changes [32]. Probiotics produce antimicrobial substances that compete with other gut microbes for nutrients and binding sites. ...
Article
Full-text available
Compounds that have negative effects on the endocrine system are called endocrine disrupting compounds (EDCs). There are several different types of compounds, with several different usage areas in the environment, which can be classified as EDCs. These chemicals have a wide range of negative health effects in organisms, depending on their target hormone system. EDCs are among the most popular topics of scientific research, as they are widely used and organisms are frequently exposed to these chemicals. There are various exposure routes for EDCs, such as oral, inhalation and dermal exposure. Parabens, phenolic compounds, phthalates, and pesticides are the most common EDCs. Nowadays, intestinal microorganism distribution, probiotics, and food supplements that regulate these microorganisms and their protective effects against various harmful chemicals attract attention. For this reason, many studies have been carried out in this field and certain diet schemes have been created according to the results of these studies. In fact, probiotics are preferred in order to reduce and eliminate the negative effects of harmful chemicals and to ensure that the organism reacts strongly in these conditions. In this review, we will focus on EDCs, their health effects and positive effects of probiotics on EDCs exposure conditions.
... Imbalance in the microbiome has been linked with health issues in many animals, including humans (Shreiner et al., 2015). One major contributor to an imbalanced microbiome in the gastrointestinal tract is pesticide pollutants in food (Yuan et al., 2019). Recently, it was shown that the widely used herbicide glyphosate can reduce the diversity of the gut microbiome in honeybees (Motta et al., 2018). ...
Article
Full-text available
• Insect diversity and biomass have been declining around the world. This might have severe consequences on the environment since insects provide many crucial ecosystem services. One major driver behind the decline is continuous pesticide use which also affects nontarget organisms. Even at low doses, chronic exposure to pesticides may have negative long-term effects. Ants have not received much attention in this context, despite their importance in terrestrial ecosystems. • A full factorial experimental design was used to test how ingestion of two widely used pesticides influence colonies of the ant Cardiocondyla obscurior. Colonies were exposed for 12 weeks to the herbicide glyphosate and the neonicotinoid insecticide thiacloprid, separately and in combination. Brood production and the size of new workers and queens produced in these colonies were measured. In addition, the relative densities of two endosymbionts were quantified and immunocompetence tested by measuring survival after fungal infection. • The two pesticides in combination decreased brood production, which was measured as the number of produced eggs and pupae. Workers and queens produced in pesticide-exposed colonies differed in body size from individuals produced in control colonies. Furthermore, endosymbiont densities decreased after glyphosate exposure. Neither pesticide influenced survival after fungal infection. • The results show that chronic exposure to two widely used pesticides causes apparent trade-offs in reproduction and other physiological traits of ants, potentially decreasing fitness. Even low levels of pesticides in the environment may therefore have negative effects on ant colonies, contributing to the worldwide insect decline.
... Les altérations induites par les polluants des bactéries intestinales sont susceptibles de contribuer à leur toxicité [30]. Les pesticides pourraient altérer la composition du microbiote intestinal et les métabolites comme les acides biliaires et les acides gras à chaîne courte [31]. La relation avec le microbiote est dualiste. ...
Article
Full-text available
Résumé Le rôle clef du microbiote intestinal sur la santé et son lien avec l’alimentation est maintenant démontré. On sait que ses besoins sont spécifiques : les fibres et certains acides gras à longue chaîne (oméga-3) ont un effet favorable sur sa diversité et son fonctionnement, mais leur déficit, de même que certains résidus de pesticides, émulsifiants et édulcorants, entraînent une dysbiose intestinale. Or au cours des cinquante dernières années, les changements dans l’alimentation des animaux d’élevage, dans la protection des cultures (pesticides), de même que l’offre croissante en produits prêts à consommer et l’évolution induite dans les préférences des consommateurs, ont été sources de perturbations du microbiote. A tel point que 90 pour cent des Français manquent d’omégas 3 et que les produits ultra-transformés représentent 35 % des calories consommées. Une santé reposant sur un microbiote sain nécessite un changement de paradigme dans la façon de se nourrir. Pour cela il faut agir à tous les maillons du système alimentaire, par une révision de certaines pratiques agricoles et de l’industrie agroalimentaire afin d’améliorer l’offre en produits de qualité, mais aussi par un vaste effort d’éducation et de formation pour aider aux choix des aliments et à la composition des menus.
... Intestinal cells provided a natural barrier to prevent infiltration of toxic substances and pathogens. Pesticides are absorbed into body via the intestine after their administration [45], affecting the structure and enzyme activity of the intestine, and impairing the absorptive function of the intestine [46,47]. Histological results showed that rats exhibited a significant decrease in villus length from IMI and ACE exposure, which indicated that neonicotinoids tend to alter the intestinal structure, potentially leading to intestinal disorders and nutrient absorption effects. ...
Article
Full-text available
Probiotics have been shown to have positive effects when it comes to combating various health issues when consumed, preventing even the absorption of environmental toxins. One of the main environmental toxins encountered today is pesticide residues. Neonicotinoids, widely applied today in countries that have approved of them, are a known class of insecticides with an excellent and effective potency. Neonicotinoids have been shown to cause various toxic effects, either acutely or chronically, on human health and on beneficial insects when exposed. To clarify the assumption that probiotics could counteract these toxic effects, especially on vital organs, the probiotic yeast “Saccharomyces boulardii” (S. boulardii) was tested against the neonicotinoids, acetamiprid (ACE) and imidacloprid (IMI), as it has outstanding physiological and metabolic properties. The results obtained from the studies indicated that although ACE and IMI induced liver, kidney, brain and bowel damage, there was a considerable level of protection by the dietary supplementation of S. boulardii, as it reduced the absorption of these insecticides.
Article
Imidacloprid (IMI), one of the most frequently used neonicotinoid insecticides in agriculture, is resided in surface water worldwide and poses a threat to aquatic organisms. Melatonin (MT) provides effective protection against insecticide-induced toxicity, nevertheless, the toxic effects and whether MT attenuates intestinal injury caused by IMI exposure in the common carps remains poorly explored. Previous studies have reported adverse effects of IMI exposure on intestinal health status. Therefore, we first demonstrated that IMI altered the composition and function of the intestinal microbiota, destroying the integrity of intestinal ultrastructure, increasing intestinal permeability. Meanwhile, metagenomic sequencing and ELISA kits results hypothesized that peptidoglycan (PGN) is an IMI-triggered intestinal microbial metabolite. Subsequently, we thus further elucidated that IMI induced an increase in intestinal tight junction permeability by inducing PGN secretion in vitro model. MT addition dramatically attenuated IMI-induced intestinal toxicity by remitting PGN synthesis and thus resecuring tight junction permeability, thereby reducing intestinal injury. SB203580 was supplied as a P38MAPK inhibitor to alleviate the increased permeability of tight junctions induced by IMI/PGN. Therefore, these findings confirmed that MT protects against IMI-induced intestinal injury by negatively regulating PGN/P38MAPK pathway to antagonize the increased tight junction permeability.
Article
Full-text available
Microplastics are persistent and complex contaminants that have recently been found in freshwater systems, raising concerns about their presence in aquatic organisms. Plastics tend to be seen as an inert material; however, it is not well known if exposure to plastics for a prolonged time, in combination with organic chemicals, causes organism mortality. Ingestion of microplastics in combination with another pollutant may affect a host organism's fitness by altering the host microbiome. In this study, we investigated how microplastics interact with other pollutants in this multi-stress system, and whether they have a synergistic impact on the mortality of an aquatic organism and its microbiome. We used wild water boatmen Hemiptera (Corixidae) found at lake Erken located in east-central Sweden in a fully factorial two-way microcosm experiment designed with polystyrene microspheres and a commonly used detergent. The microplastic-detergent interaction is manifested as a significant increase in mortality compared to the other treatments at 48 h of exposure. The diversity of the microbial communities in the water was significantly affected by the combined treatment of microplastics and the detergent while the microbial communities in the host were affected by the treatments with microplastics and the detergent alone. Changes in relative abundance in Gammaproteobacteria (family Enterobacteriaceae), were observed in the perturbed treatments mostly associated with the presence of the detergent. This confirms that microplastics can interact with detergents having toxic effects on wild water boatmen. Furthermore, microplastics may impact wild organisms via changes in their microbial communities.
Article
Imazalil (IMZ) is a fungicide recommended by the Chinese ministry of agriculture. However, recent study was observed high level of IMZ by dietary exposure in pregnant women. To determine the cross-generational effects, C57BL/6 mice were exposed to IMZ at dietary levels of 0, 0.025‰, and 0.25‰ during the gestation and lactation periods. Then, we assessed the changes in growth phenotypes, carnitine levels, and gut microbiota in F0, F1 or F2 generations. The growth phenotypes of dams didn't observe significant difference, but there were significant changes in the offspring. Plasma samples revealed low levels of free carnitine (C0), long-chain acyl-carnitines and total carnitine. In particular, C0 may be regarded as relatively potential, specific markers by maternal IMZ exposure. Caco2 cell culture and animal experiment confirmed IMZ affected carnitine absorption through the organic cation transporter type-2 (OCTN2) protein encoded by solute carrier family 22A member 5 (SLC22A5) gene in colon. Maternal IMZ exposure also had a greater effect on gut microbiota in offspring, especially anaerobic bacteria, which positively correlated with C0 and acyl-carnitines. These results suggested that maternal IMZ exposure affected carnitine absorption through OCTN2 protein, which led to the decline of anaerobic bacteria and unbalanced intestinal homeostasis.
Article
Atrazine, a widely used herbicide, is a potential threat to the intestines of animals due to its long-term persistence in water and accumulation in animal tissues, but the underlying mechanism is unclear. In this study, we evaluated the toxicity of atrazine (50, 100, and 500 µg/L) on the intestine of Pelophylax nigromaculatus larvae from Gosner stages 18–42 (about 90 days). We conducted a 16 S rRNA gene amplification study, which showed that chronic exposure to atrazine changed the diversity and composition of intestinal microbiota of P. nigromaculatus larvae. Chronic exposure to atrazine (50, 100, and 500 µg/L) significantly decreased the relative abundance of Fusobacteria and U114, while 50 µg/L and 100 µg/L atrazine resulted in a significant increase of Clavibacter. The LC-MS/MS metabolomics indicated that there were 145 significantly changed metabolites. Furthermore, atrazine led to metabolic abnormalities related to purine metabolism and biosynthesis of amino acids in the intestine. The transcriptomic results showed that atrazine exposure caused 21,120 differentially expressed genes between the control and the atrazine exposure groups. Atrazine exposure primarily disturbed the pathways related to the cytokine-cytokine receptor interaction and cell adhesion molecules. Moreover, 500 µg/L atrazine caused a significant up-regulation in the gene expression of apolipoprotein (ApoA1, ApoB, and ApoA4), and fatty acid binding protein (FABP1), as well as a significant down-regulation in the gene expression of superoxide dismutase (SOD). Our work provides insight into the ecotoxicity mechanisms of atrazine in amphibians at the level of intestinal microbiota response, metabolome and transcriptome, and serves as a basis for future research on pesticide pollutants.
Chapter
Glyphosate is the active ingredient of many widely used herbicides. It targets 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), whose lack in humans confers low toxicity to glyphosate-based herbicides (GBHs). Nevertheless, its use is currently a debated topic. Several studies indicating toxicity are emerging, including associations between glyphosate and immune-endocrine disturbances. This chapter aims to describe the possible correlation between GBH exposure and immune-endocrine alterations. Data suggest that GBHs should be considered endocrine-disrupting compounds with effects on sex and thyroid hormones. Evidence of immune system alteration are fewer, but highlighted possible noxious effects on it, including lung inflammation, rhinitis, and celiac disease. An attractive hypothesis could be the one that connects microbiome dysbiosis, as several microorganisms express EPSPS and may be affected by glyphosate, and thus subsequent immune-endocrine alterations. Considering the wide use of GBHs, critical analyses are required to better characterize safety profile and possible health consequences of immune-endocrine alterations.
Article
The development of an individual during fetal life and childhood is characterized by rapid growth as well as gradual maturation of organs and systems. Beyond the nutritional intake in essential nutrients, food contaminants can permanently influence the way organs mature and function. These processes are called “programming” and play an essential role in the occurrence of non-communicable chronic diseases throughout the lifespan. Populations as pregnant women, fetuses and young children are vulnerable and particularly sensitive to food contaminants which can induce epigenetic modifications transmissible to future generations. Among these contaminants, pesticides are found in most food matrices exposing humans to cocktails of molecules through variable concentrations and duration of exposure. The Maillard reaction products (MRPs) represent other food contaminants resulting from heat treatment of food. Modern diet, rich in fats and sugars, is also rich in neoformed pathogenic compounds, Advanced Glycation End products (AGEs), the levels of which depend on the heat treatment of foods and eating habits and whose effects on health are controversial. In this review, we have chosen to present the current knowledge on the impacts of selected pesticides and MRPs, on the risk of developing during life non-communicable chronic diseases such as IBD, metabolic disorders or allergies. A large review of literature was performed via Pubmed, and the most appropriate studies were summarised.
Article
Environmental risks caused by emerging per- and polyfluoroalkyl substances (PFASs) have attracted increasing attention. As an important substitute for perfluorooctane sulfonate (PFOS), sodium p-perfluorous nonenoxybenzene sulfonate (OBS) is widely used as a firefighting foam additive and oil recovery agent in China. This study reported the tissue distribution of OBS in KM mice that were administered a dose of OBS at 10 µg/day via daily oral gavage for 7, 14, or 28 days. During exposure, gender-based differences were observed in body weight changes and tissue distribution of OBS. Liver exhibited the highest concentrations (males: 12.57±1.80 µg/g; females: 11.80±5.32 µg/g) and tissue/blood ratios and contributed more than 50% to the whole-body burden of OBS in both male and female mice, showing its ability to enrich PFASs. Furthermore, there were certain differences in the distribution characteristics of the three OBS isomers. Based on its bioaccumulation potential and widespread use, further studies are required on the human exposure risks of OBS.
Article
Chemically intensive crop production depletes wildlife food resources, hinders animal development, health, survival, and reproduction, and it suppresses wildlife immune systems, facilitating emergence of infectious diseases with excessive mortality rates. Gut microbiota is crucial for wildlife's response to environmental stressors. Its composition and functionality are sensitive to diet changes and environmental pollution associated with modern crop production. In this study we use shotgun metagenomics (median 8,326,092 sequences/sample) to demonstrate that exposure to modern crop production detrimentally affects cecal microbiota of sharp-tailed grouse (Tympanuchus phasianellus: 9 exposed, 18 unexposed and greater prairie chickens (T. cupido; 11, 11). Exposure to crop production had greater effect on microbiota richness (t = 6.675, P < 0.001) and composition (PERMANOVA r² = 0.212, P = 0.001) than did the host species (t = 4.762, P < 0.001; r² = 0.070, P = 0.001) or their interaction (t = 3.449; r² = 0.072, both P = 0.001), whereas sex and age had no effect. Although microbiota richness was greater in exposed (T. cupido chao1 = 152.8 ± 20.5; T. phasianellus 115.3 ± 17.1) than in unexposed (102.9 ± 15.1 and 101.1 ± 17.2, respectively) birds, some beneficial bacteria dropped out of exposed birds' microbiota or declined and were replaced by potential pathogens. Exposed birds also had higher richness and load of virulome (mean ± standard deviation; T. cupido 24.8 ± 10.0 and 10.1 ± 5.5, respectively; T. phasianellus 13.4 ± 6.8/4.9 ± 2.8) and resistome (T. cupido 46.8 ± 11.7/28.9 ± 10.2, T. phasianellus 38.3 ± 16.7/18.9 ± 14.2) than unexposed birds (T. cupido virulome: 14.2 ± 13.5, 4.5 ± 4.2; T. cupido resistome: 31.6 ± 20.2 and 13.1 ± 12.0; T. phasianellus virulome: 5.2 ± 4.7 and 1.4 ± 1.5; T. phasianellus resistome: 13.7 ± 16.1 and 4.0 ± 6.4).
Article
Background Toxicology studies suggest that neonicotinoids may be associated with adiposity development via thyroid hormone disruption and increased oxidative stress. Prior epidemiological studies report mixed results for the association between neonicotinoids and adiposity measures. Objective To examine the association between detectable concentrations of parent neonicotinoids (imidacloprid, acetamiprid, clothianidin) and neonicotinoid metabolites (5-hydroxy-imidacloprid, N-desmethyl-acetamiprid) with adiposity measures among US adults, and whether sex modifies the associations for metabolites. Methods National Health and Nutrition Examination Survey (NHANES) 2015–2016 data was utilized to estimate covariate adjusted associations between detectable neonicotinoids and fat mass index (FMI), lean mass index (LMI), waist circumference, body fat percentage, and body mass index (BMI) using multiple linear regression. The odds of being overweight or obese with detectable neonicotinoids were estimated using logistic regression. Sampling strategies were accounted for in the regression models. Results Detectable levels of acetamiprid were associated with a decrease in FMI (β = −3.33 kg/m², 95% CI [-5.31, −1.36]), LMI (β = −3.36 kg/m², 95% CI [-5.63, −1.09]), body fat percentage (β = −4.57, 95% CI [-8.73, −0.40]), waist circumference (β = −10.62 cm, 95% CI [-20.57, −0.68]), and BMI (β = −4.25 kg/m², 95% CI [-7.57, −0.92]) among adults. In contrast, detectable levels of 5-hydroxy-imidacloprid were associated with greater odds of being overweight or obese (OR = 1.53, 95% CI [1.17, 1.99]) and increased LMI (β = 0.65 kg/m², 95% CI [0.06, 1.24]). Sex modified the association between N-desmethyl-acetamiprid and LMI (pint = 0.090) with positive association among males (β = 1.05 kg/m², 95% CI [0.22, 1.87]), and insignificant inverse associations in females. Sex also modified the association for N-desmethyl-acetamiprid with FMI (pint = 0.095) and body fat percentage (pint = 0.072), with suggestive evidence showing positive associations for males and inverse associations for females. Conclusion In this exploratory analysis, detectable concentrations of acetamiprid were inversely associated with adiposity, while there were mixed findings for 5-hydroxy-imidacloprid. Findings suggest sex differences, though results are not clear with regard to the directionality of the association by sex.
Chapter
Climate change affects the health of human beings through several mechanisms. Changes in the average surface temperature on earth, heat waves, adverse weather events and other environmental alterations can increase mortality and morbidity by increasing the risk of infections carried by food and water. Water-related diseases could occur due to both the deficiency of water and its poor quality. They are generally classified into four groups: waterborne, water-washed, water-based and water-related vector-borne diseases. Food-borne diseases can be achieved either by ingesting the pathogenic microorganism or through the toxins produced by them contained in the food. Furthermore, ecological and environmental changes directly affect the spread of vector-borne diseases that nowadays continue representing some of the major microbial causes of morbidity and mortality in the world.Environmental alterations associated with climate change have also been proved to influence microbial communities within the human body. This diverse community that colonize us has demonstrated importance on the function of the immune system, food digestion, development of chronic diseases and modulation of brain functioning. It is being affected by elements such as antibiotic use, heavy metals, micro-plastics, organic pollutants, pesticides and food additives. Through all these mechanisms, among yet so many others, climate change is affecting human health.KeywordsClimate changeEnvironmentHuman microbiotaWaterborne diseasesVector-borne diseasesFood-borne diseasesPollution
Article
Prochloraz (PCZ), an imidazole fungicide, has been extensively used in horticulture and agriculture to protect against pests and diseases. To investigate the potential toxicity of PCZ on aquatic organisms, larval zebrafish, as a model, were exposed to a series of concentrations (0, 20, 100, and 500 μg/L) of PCZ for 7 days. With transcriptomic analysis, we found that exposure to high dose PCZ could produce 76 downregulated and 345 upregulated differential expression genes (DEGs). Bioinformatics analysis revealed that most of the DEGs were characterized in the pathways of glycolipid metabolism, amino acid metabolism and oxidative stress in larval zebrafish. Targeted metabolomic analysis was conducted to verify the effects of PCZ on the levels of acyl-carnitines and some amino acids in larval zebrafish. In addition, biochemical indicators related to glycolipid metabolism were affected obviously, manifested as elevated triglyceride (TG) levels and decreased glucose (Glu) levels in whole larvae. The expression levels of genes associated with glycolipid metabolism were affected in larvae after exposure to PCZ (PK, GK, PEPckc, SREBP, ACO). Interestingly, we further confirmed that PCZ could induce oxidative stress by the changing enzyme activities (T-GSH, GSSG) and upregulating several related genes levels in larval zebrafish. Generally, our results revealed that the endpoints related to glycolipid metabolism, amino acid metabolism and oxidative stress were influenced by PCZ in larval zebrafish.
Article
The gut microbiota contributes to diverse aspects of host physiology, ranging from immunomodulation to drug metabolism. Changes in the gut microbiota composition are associated with various diseases as well as with the response to medications. It is therefore important to understand how different lifestyle and environmental factors shape gut microbiota composition. Beyond the commonly considered factor of diet, small-molecule drugs have recently been identified as major effectors of the microbiota composition. Other xenobiotics, such as environmental or chemical pollutants, can also impact gut bacterial communities. Here, we review the mechanisms of interactions between gut bacteria and antibiotics, host-targeted drugs, natural food compounds, food additives and environmental pollutants. While xenobiotics can impact bacterial growth and metabolism, bacteria in turn can bioaccumulate or chemically modify these compounds. These reciprocal interactions can manifest in complex xenobiotic–microbiota–host relationships. Our Review highlights the need to study mechanisms underlying interactions with pollutants and food additives towards deciphering the dynamics and evolution of the gut microbiota. We take up a multitude of foreign substances, so called xenobiotics, such as medications, food additives and pollutants, which affect the composition and function of the gut microbiota. In this Review, Lindell, Zimmermann-Kogadeeva and Patil discuss these reciprocal interactions and their mechanisms.
Chapter
With rising environmental pollution and overuse of chemicals, the effect of emerging contaminants on human health is one of the major concerns. Human beings are exposed to various toxic chemicals like pesticides, perfluorinated chemicals, microplastics, 1,4 dioxins, and trihalomethane in occupational and environmental settings. According to the Fourth Report on Human Exposure to Environmental Chemicals, 2019, published by Centers for Disease Control and Prevention, detectable levels of 50 pesticides have been found in the body fluids of a representative sample of the United States population. These pesticides not only cause detrimental effects on human physiology but also induce long-term transgenerational effects. A large number of pesticides like permethrin, methoxychlor, and Dichlorodiphenyltrichloroethane have been reported to promote epigenetic alterations in rodent models. All such epigenetic and possible aneugenic change can serve as driving forces for evolution. Herein, we focus on the short-term effect of pesticides on human physiology, long-term epigenetic effects, and their evolutionary consequences.
Preprint
Full-text available
Background: Microplastics are a pervasive pollutant widespread in the sea and freshwater from anthropogenic sources, and together with the presence of pesticides, they can have physical and chemical effects on aquatic organisms and on their microbiota. Few studies have explored the combined effects of microplastics and pesticides on the host-microbiome, and more importantly, the effects across multiple trophic levels. In this work, we studied the effects of exposure to microplastics and the pesticide deltamethrin on the diversity and abundance of the host-microbiome across a three-level food chain: daphnids-damselfly-dragonflies. Daphnids were the only organism exposed to 1µm microplastic beads, and they were fed to damselfly larvae. Those damselfly larvae were exposed to deltamethrin and then fed to the dragonfly larvae. The microbiotas of the daphnids, damselflies, and dragonflies were analyzed. Results: Our results suggest that the exposure to microplastics and deltamethrin had negative carry-over effects on the diversity and abundance of the microbiome across the three trophic levels. Moreover, the exposure to deltamethrin on the damselflies negatively affected their survival rate in the presence of the dragonfly predator, but no such effects were found on damselflies exposed to only microplastics. Conclusions: Our study highlights the importance of evaluating ecotoxicological effects at the community level. Importantly, the indirect exposure to microplastics and pesticides through diet can potentially have bottom-up effects on the trophic webs.
Article
The widespread use of chlorothalonil (CTL) has caused environmental residues and food contamination. Although the intestinal epithelial barrier (IEB) is directly involved in the metabolism and transportation of various exogenous compounds, there are few studies on the toxic effects of these compounds on the structure and function of IEB. The disassembly of tight junction (TJ) is a major cause of intestinal barrier dysfunction under exogenous compounds intake, but the precise mechanisms are not well understood. Here, we used Caco-2 cell monolayers as an in vitro model of human IEB to evaluate the toxicity of CTL exposure on the structure and function of IEB. Results showed that CTL exposure increased the paracellular permeability of the monolayers and downregulated messenger RNA levels of the TJ genes (ZO-1, OCLN, and CLDN1), polarity marker gene (SI), and anti-apoptosis gene (BCL-2) but upregulated the messenger RNA levels of apoptosis-related genes, including BAD, BAX, CASP3, and CASP8. Western blot analysis and immunofluorescence assay results showed the decreased levels and disrupted distribution of TJ protein network, including ZO-1 and CLDN1 in CTL-exposed IEB. In addition, the accumulation of intracellular reactive oxygen species, decreased mitochondrial membrane potential, and increased active CASP3 expression were observed in treated IEB. The result of TUNEL assay further confirmed the occurrence of cell apoptosis after CTL exposure. In addition, the phosphorylation of mitogen-activated protein kinases, including ERK, JNK and p38, was increased in CTL-exposed IEB. In summary, our results demonstrated that CTL exposure induced IEB dysfunction in Caco-2 cell monolayers by activating the mitogen-activated protein kinase pathway.
Chapter
Pesticides have grown as an inseparable part of crop production and possess applications in agricultural activities worldwide. But the pesticide residues leach out from point source and make their ways into water bodies, which is of global concern. These pesticides are mostly synthetic chemicals having properties to kill the targeted organisms, but they can also affect the nontarget organisms. These compounds exhibit toxic properties, high perseverance, and bioaccumulation, which necessitates their removal. Several pesticides are highly toxic and have long half-lives, some for many years, and many of them are listed as persistent organic pollutants/pesticides by the Stockholm Convention. Water is a vital environmental matrix for life existence and the pesticide contamination of water can lead to tremendous health issues. To overcome the threat of the health risks posed by these contaminants, it is important to devise potent detection and treatment strategies. This chapter articulates the current scenario of different pesticides contaminating the water resources. It also summarizes the health risks posed by them and the various point sources contributing to their elevated level in water bodies. Importantly, it will also add light on the emerging pesticides being used unregulated in agricultural and other activities, and thus making their ways into water bodies.
Article
Propamocarb is a systemic carbamate fungicide used to fight diseases. The effect of propamocarb on the formation of atherosclerosis was evaluated in wild-type (WT) and ApoE knockout (ApoE−/−) mice. C57BL/6 J WT mice were fed control diet or high-fat diet (HFD) with 20 mg/L propamocarb in drinking water for 24 weeks. Propamocarb significantly increased the serum levels of triglyceride, cholesterol and low-density lipoprotein cholesterol while decreasing high-density lipoprotein cholesterol. Simultaneously, propamocarb facilitated lipid accumulation in the liver and increased the expression of cholesterol synthesis and transport genes in the liver and ileum. Lipid accumulation was observed in the aortic roots of the propamocarb-treated mice fed HFD, and similar results were also observed with whole aorta staining. In addition, propamocarb exposure significantly increased the mRNA levels of IL-1β, TNF-α, ICAM-1, and VCAM-1 in the aorta and the serum IL-1β, IL-6, and TNF-α levels in HFD groups treated with propamocarb. In ApoE−/− mice, the results were consistent with those obtained in WT mice after exposure to 20 mg/L propamocarb for 10 weeks. Meanwhile, propamocarb significantly increased the levels of CD36, NF-κB, VCAM-1 and ICAM-1 proteins in the aortas of ApoE−/− mice. Propamocarb further disrupted cholesterol metabolism and enhanced atherosclerosis and inflammatory responses much more substantially, indicating that propamocarb has the potential to accelerate the formation of atherosclerosis. An analysis of gut microbiota revealed that propamocarb altered the composition of gut microbiota in both WT and ApoE−/− mice. Interestingly, propamocarb increased the abundance of Peptostreptococcaceae, Ruminococcaceae, and Clostridiales_VadinBB60_group, which are related to atherosclerosis at the family level. The abundance of Paeniclostridium, Allobaculum, and Clostridioides, which are closely related to atherosclerosis, was also increased by propamocarb exposure. Our findings indicate that propamocarb exposure may promote atherosclerosis by disrupting lipid metabolism, increasing the inflammatory response, and altering the structure of gut microbiota.
Article
Full-text available
Environmental chemicals can alter gut microbial community composition, known as dysbiosis. However, the gut microbiota is a highly dynamic system and its functions are still largely underexplored. Likewise, it is unclear whether xenobiotic exposure affects host health through impairing host–microbiota interactions. Answers to this question not only can lead to a more precise understanding of the toxic effects of xenobiotics but also can provide new targets for the development of new therapeutic strategies. Here, we aim to identify the major challenges in the field of microbiota-exposure research and highlight the need to exam the health effects of xenobiotic-induced gut microbiota dysbiosis in host bodies. Although the changes of gut microbiota frequently co-occur with the xenobiotic exposure, the causal relationship of xenobiotic-induced microbiota dysbiosis and diseases is rarely established. The high dynamics of the gut microbiota and the complex interactions among exposure, microbiota, and host, are the major challenges to decipher the specific health effects of microbiota dysbiosis. The next stage of study needs to combine various technologies to precisely assess the xenobiotic-induced gut microbiota perturbation and the subsequent health effects in host bodies. The exposure, gut microbiota dysbiosis, and disease outcomes have to be causally linked. Many microbiota–host interactions are established by previous studies, including signaling metabolites and response pathways in the host, which may use as start points for future research to examine the mechanistic interactions of exposure, gut microbiota, and host health. In conclusion, to precisely understand the toxicity of xenobiotics and develop microbiota-based therapies, the causal and mechanistic links of exposure and microbiota dysbiosis have to be established in the next stage study.
Article
Full-text available
Background Disruption of the gut microbiota homeostasis may induce low-grade inflammation leading to obesity-associated diseases. A major protective mechanism is to use the multi-layered mucus structures to keep a safe distance between gut epithelial cells and microbiota. To investigate whether pesticides would induce insulin resistance/obesity through interfering with mucus-bacterial interactions, we conducted a study to determine how long-term exposure to chlorpyrifos affected C57Bl/6 and CD-1 (ICR) mice fed high- or normal-fat diets. To further investigate the effects of chlorpyrifos-altered microbiota, antibiotic treatment and microbiota transplantation experiments were conducted. Results The results showed that chlorpyrifos caused broken integrity of the gut barrier, leading to increased lipopolysaccharide entry into the body and finally low-grade inflammation, while genetic background and diet pattern have limited influence on the chlorpyrifos-induced results. Moreover, the mice given chlorpyrifos-altered microbiota had gained more fat and lower insulin sensitivity. Conclusions Our results suggest that widespread use of pesticides may contribute to the worldwide epidemic of inflammation-related diseases. Electronic supplementary material The online version of this article (10.1186/s40168-019-0635-4) contains supplementary material, which is available to authorized users.
Article
Full-text available
Background Antibiotics are commonly used worldwide, and pesticide is a kind of xenobiotic to which humans are frequently exposed. The interactive impact of antibiotics on pesticides has rarely been studied. We aim to investigate the effects of antibiotics on the pesticide exposure risk and whether gut microbiota altered by antibiotics has an influence on pesticide bioavailability. Furthermore, we explored the mechanisms of gut microbiota affecting the fate of pesticides in the host. Results The oral bioavailability of triazine herbicides significantly increased in the rats treated with ampicillin or antibiotic cocktails. The antibiotic-altered gut microbiota directly influenced the increased pesticide bioavailability through downregulating hepatic metabolic enzyme gene expression and upregulating intestinal absorption-related proteins. Conclusions Antibiotics could increase the pesticide bioavailability and thereby may increase the pesticide exposure risk. The antibiotic-altered gut microbiota that could alter the hepatic metabolic enzyme gene expression and intestinal absorption-related proteome was a critical cause of the increased bioavailability. This study revealed an undiscovered potential health impact of antibiotics and reminded people to consider the co-exposed xenobiotics when taking antibiotics. Electronic supplementary material The online version of this article (10.1186/s40168-018-0602-5) contains supplementary material, which is available to authorized users.
Article
Full-text available
The gut microbiome is highly involved in numerous aspects of host physiology, from energy harvest to stress response, and can confer many benefits to the host. The gut microbiome development could be affected by genetic and environmental factors, including the pesticides. The carbamate insecticide aldicarb has been extensively used in agriculture, which raises serious public health concern. However, the impact of aldicarb on the gut microbiome, host metabolome and lipidome has not been well studied yet. Herein, we use multi-omics approaches, including16S rRNA sequencing, shotgun metagenomics sequencing, metabolomics and lipidomics, to elucidate aldicarb-induced toxicity in the gut microbiome and the host metabolic homeostasis. We demonstrated that aldicarb perturbed the gut microbiome development trajectory, enhanced gut bacterial pathogenicity, altered complex lipid profile, induced oxidative stress, protein degradation and DNA damage. The brain metabolism was also disturbed by the aldicarb exposure. These findings may provide a novel understanding of the toxicity of carbamate insecticides.
Article
Full-text available
The intestinal microbiota and insulin sensitivity are rapidly altered after ingestion of obesogenic diets. We find that changes in the composition of the fecal microbiota precede changes in glucose tolerance when mice are fed obesogenic, low fiber, high fat diets (HFDs). Antibiotics alter glycemia during the first week of certain HFDs, but antibiotics show a more robust improvement in glycemic control in mice with protracted obesity caused by long-term feeding of multiple HFDs. Microbiota transmissible dysglycemia and glucose intolerance only occur when germ-free mice are exposed to obesity-related microbes for more than 45 days. We find that sufficient host exposure time to microbiota derived from HFD-fed mice allows microbial factors to contribute to insulin resistance, independently from increased adiposity in mice. Our results are consistent with intestinal microbiota contributing to chronic insulin resistance and dysglycemia during prolonged obesity, despite rapid diet-induced changes in the taxonomic composition of the fecal microbiota.
Article
Full-text available
Growing evidence indicates that the human gut microbiota interacts with xenobiotics, including persistent organic pollutants and foodborne chemicals. The toxicological relevance of the gut microbiota-pollutant interplay is of great concern since chemicals may disrupt gut microbiota functions, with a potential impairment of host homeostasis. Herein we report within batch fermentation systems the impact of food contaminants (polycyclic aromatic hydrocarbons, polychlorobiphenyls, brominated flame retardants, dioxins, pesticides and heterocyclic amines) on the human gut microbiota by metatranscriptome and volatolome i.e. "volatile organic compounds" analyses. Inflammatory host cell response caused by microbial metabolites following the pollutants-gut microbiota interaction, was evaluated on intestinal epithelial TC7 cells. Changes in the volatolome pattern analyzed via solid-phase microextraction coupled to gas chromatography-mass spectrometry mainly resulted in an imbalance in sulfur, phenolic and ester compounds. An increase in microbial gene expression related to lipid metabolism processes as well as the plasma membrane, periplasmic space, protein kinase activity and receptor activity was observed following dioxin, brominated flame retardant and heterocyclic amine exposure. Conversely, all food contaminants tested induced a decreased in microbial transcript levels related to ribosome, translation and nucleic acid binding. Finally, we demonstrated that gut microbiota metabolites resulting from pollutant disturbances may promote the establishment of a pro-inflammatory state in the gut, as stated with the release of cytokine IL-8 by intestinal epithelial cells.
Article
Full-text available
Effects of glyphosate on survival, developmental rate, larval weight, and midgut bacterial diversity of Apis mellifera were tested in the laboratory. Larvae were reared in vitro and fed diet containing glyphosate 0.8, 4, and 20 mg/L. The dependent variables were compared with negative control and positive control (dimethoate 45 mg/L). Brood survival decreased in 4 or 20 mg/L glyphosate treatments but not in 0.8 mg/L, and larval weight decreased in 0.8 or 4 mg/L glyphosate treatments. Exposure to three concentrations did not affect the developmental rate. Furthermore, the intestinal bacterial communities were determined using high-throughput sequencing targeting the V3–V4 regions of the 16S rDNA. All core honey bee intestinal bacterial phyla such as Proteobacteria (30.86%), Firmicutes (13.82%), and Actinobacteria (11.88%) were detected, and significant changes were found in the species diversity and richness in 20 mg/L glyphosate group. Our results suggest that high concentrations of glyphosate are deleterious to immature bees.
Article
Full-text available
Endocrine-disrupting chemicals (EDC) are widespread in the built and natural environments. Heightened public awareness of their potential danger has led to concern about whether EDC and their metabolites have significant negative biological effects. Studies have shown that EDC like DDT and other organochlorine pesticides, such as methoxychlor (MXC), have adverse effects on immune cells, but no studies have addressed the impact of HPTE, the primary metabolite of MXC. To elucidate the presence and significance of HPTE adverse effects, this study explored the impact of HPTE on a critical window and component of immune system development, embryonic T-cell development. Lesions at this phase of development can lead to lifelong immune dysfunction and increased incidence of immune disease, such as autoimmunity. Embry-onic thymocytes (GD 16-18) from C57BL/6 mice were subjected to an in vitro differentiation culture that mimicked early steps in thymocyte development in the presence of 0.005, 0.05, 0.5, 5, or 50 μM HPTE, or a model endocrine disruptor, DES. The results indicated that compared to the vehicle control, HPTE- and DES-induced death of thymocytes. Annexin-V staining and Caspase 8, markers of programed cell death, revealed that the loss of cells was due at least in part to induction of apoptosis. Moreover, HPTE-induced cell death not only resulted in selective loss of double positive thymocytes, but also loss of developing CD4 intermediate cells (post-double positive partially differentiated thymocyte population). Phenotypic analysis of thymocyte maturation (T-cell receptor, TCR) and TCR ligation (CD5) surface markers revealed that surviving embryonic thymocytes expressed low levels of both. Taken together these data demonstrate that immature embryonic thymocytes are sensitive to HPTE exposure and that HPTE exposure targets thymocyte populations undergoing critical differentiation steps. These findings suggest HPTE may play a pivotal role in MXC exposure-induced immune dysfunction.
Article
Full-text available
Background: Epidemiological evidence suggests a link between pesticide exposure and the development of metabolic diseases. However, most experimental studies have evaluated the metabolic effects of pesticides using individual molecules, often at nonrelevant doses or in combination with other risk factors such as high-fat diets. Objectives: We aimed to evaluate, in mice, the metabolic consequences of chronic dietary exposure to a pesticide mixture at nontoxic doses, relevant to consumers' risk assessment. Methods: A mixture of six pesticides commonly used in France, i.e., boscalid, captan, chlorpyrifos, thiofanate, thiacloprid, and ziram, was incorporated in a standard chow at doses exposing mice to the tolerable daily intake (TDI) of each pesticide. Wild-type (WT) and constitutive androstane receptor-deficient (CAR-/-) male and female mice were exposed for 52 wk. We assessed metabolic parameters [body weight (BW), food and water consumption, glucose tolerance, urinary metabolome] throughout the experiment. At the end of the experiment, we evaluated liver metabolism (histology, transcriptomics, metabolomics, lipidomics) and pesticide detoxification using liquid chromatography-mass spectrometry (LC-MS). Results: Compared to those fed control chow, WT male mice fed pesticide chow had greater BW gain and more adiposity. Moreover, these WT males fed pesticide chow exhibited characteristics of hepatic steatosis and glucose intolerance, which were not observed in those fed control chow. WT exposed female mice exhibited fasting hyperglycemia, higher reduced glutathione (GSH):oxidized glutathione (GSSG) liver ratio and perturbations of gut microbiota-related urinary metabolites compared to WT mice fed control chow. When we performed these experiments on CAR-/- mice, pesticide-exposed CAR-/- males did not exhibit BW gain or changes in glucose metabolism compared to the CAR-/- males fed control chow. Moreover, CAR-/- females fed pesticide chow exhibited pesticide toxicity with higher BWs and mortality rate compared to the CAR-/- females fed control chow. Conclusions: To our knowledge, we are the first to demonstrate a sexually dimorphic obesogenic and diabetogenic effect of chronic dietary exposure to a common mixture of pesticides at TDI levels, and to provide evidence for a partial role for CAR in an in vivo mouse model. This raises questions about the relevance of TDI for individual pesticides when present in a mixture. https://doi.org/10.1289/EHP2877.
Article
Full-text available
Background: Little is known about modifiable risk factors for thyroid disease. Several pesticides have been implicated in thyroid disruption, but clinical implications are not clear. Objective: We assessed associations between pesticide use and other farm exposures and incident hypothyroidism and hyperthyroidism in female spouses of farmers in the Agricultural Health Study (AHS). Methods: We used Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals for risk of thyroid disease in 24,092 spouses who completed at least one follow-up questionnaire. Results: We identified 1627 hypothyroid and 531 hyperthyroid cases over 20 years of follow-up. The fungicides benomyl, maneb/mancozeb, and metalaxyl, the herbicide pendimethalin, and among those over 60 years of age the insecticides parathion and permethrin (applied to crops) were associated with elevated hypothyroidism risk, with HR ranging from 1.56-2.44. Conversely, the insecticide phorate, and the herbicides imazethapyr and metolachlor were associated with decreased risk (HR ranging 0.63-0.73), as were long-term farm residence and other farm-related activities (HR ranging 0.69-0.84). For hyperthyroidism, the insecticide diazinon, the fungicides maneb/mancozeb, and the herbicide metolachlor were associated with increased risk (HR ranging 1.35-2.01) and the herbicide trifluralin with decreased risk (HR: 0.57). Conclusions: Several individual pesticides were associated with increased risk of hypothyroidism and hyperthyroidism, although some pesticides were associated with decreased risk. Some of the findings, specifically associations with fungicides, are consistent with results from an earlier analysis of prevalent diseases in AHS spouses.
Article
Full-text available
Synthetic chemicals (environmental pollutants, food additives) are widely used for many industrial purposes and consumer-related applications, which implies, through manufactured products, diet, and environment, a repeated exposure of the general population with growing concern regarding health disorders. The gastrointestinal tract is the first physical and biological barrier against these compounds, and thus their first target. Mounting evidence indicates that the gut microbiota represents a major player in the toxicity of environmental pollutants and food additives; however, little is known on the toxicological relevance of the mucus/pollutant interplay, even though mucus is increasingly recognized as essential in gut homeostasis. Here, we aimed at describing how environmental pollutants (heavy metals, pesticides, and other persistent organic pollutants) and food additives (emulsifiers, nanomaterials) might interact with mucus and mucus-related microbial species; that is, “mucophilic” bacteria such as mucus degraders. This review highlights that intestinal mucus, either directly or through its crosstalk with the gut microbiota, is a key, yet underestimated gut player that must be considered for better risk assessment and management of environmental pollution.
Article
Full-text available
Dietary exposure to the organophosphorothionate pesticide chlorpyrifos (CPF) has been linked to dysbiosis of the gut microbiota. We therefore sought to investigate whether (i) CPF’s impact extends to the intestinal barrier and (ii) the prebiotic inulin could prevent such an effect. In vitro models mimicking the intestinal environment (the SHIME®) and the intestinal mucosa (Caco-2/TC7 cells) were exposed to CPF. After the SHIME® had been exposed to CPF and/or inulin, we assessed the system’s bacterial and metabolic profiles. Extracts from the SHIME®’s colon reactors were then transferred to Caco-2/TC7 cultures, and epithelial barrier integrity and function were assessed. We found that inulin co-treatment partially reversed CPF-induced dysbiosis and increased short-chain fatty acid production in the SHIME®. Furthermore, co-treatment impacted tight junction gene expression and inhibited pro-inflammatory signaling in the Caco-2/TC7 intestinal cell line. Whereas, an isolated in vitro assessment of CPF and inulin effects provides useful information on the mechanism of dysbiosis, combining two in vitro models increases the in vivo relevance.
Article
Full-text available
Chronic kidney disease (CKD) has been shown to result in profound changes in the composition and functions of the gut microbial flora which by disrupting intestinal epithelial barrier and generating toxic by-products contributes to systemic inflammation and the associated complications. On the other hand, emerging evidence points to the role of the gut microbiota in the development and progression of CKD by provoking inflammation, proteinuria, hypertension, and diabetes. These observations demonstrate the causal interconnection between the gut microbial dysbiosis and CKD. The gut microbiota closely interacts with the inflammatory, renal, cardiovascular, and endocrine systems via metabolic, humoral, and neural signaling pathways, events which can lead to chronic systemic inflammation, proteinuria, hypertension, diabetes, and kidney disease. Given the established role of the gut microbiota in the development and progression of CKD and its complications, favorable modification of the composition and function of the gut microbiome represents an appealing therapeutic target for prevention and treatment of CKD. This review provides an overview of the role of the gut microbial dysbiosis in the pathogenesis of the common causes of CKD including hypertension, diabetes, and proteinuria as well as progression of CKD.
Article
Full-text available
Nowadays, there seems to be a consensus about the multifactorial nature of autism spectrum disorders (ASD). The literature provides hypotheses dealing with numerous environmental factors and genes accounting for the apparently higher prevalence of this condition. Researchers have shown evidence regarding the impact of gut bacteria on neurological outcomes, altering behavior and potentially affecting the onset and/or severity of psychiatric disorders. Pesticides and agrotoxics are also included among this long list of ASD-related environmental stressors. Of note, ingestion of glyphosate (GLY), a broad-spectrum systemic herbicide, can reduce beneficial bacteria in the gastrointestinal tract microbiota without exerting any effects on the Clostridium population, which is highly resistant to this herbicide. In the present study, (i) we performed a systematic review to evaluate the relationship between Clostridium bacteria and the probability of developing and/or aggravating autism among children. For that purpose, electronic searches were performed onMedline/PubMedandScielodatabases for identification of relevant studies published in English up to December 2017. Two independent researches selected the studies and analyzed the data. The results of the present systematic review demonstrate an interrelation between Clostridium bacteria colonization of the intestinal tract and autism. Finally, (ii) we also hypothesize about how environmental GLY levels may deleteriously influence the gut-brain axis by boosting the growth of Clostridium bacteria in autistic toddlers.
Article
Full-text available
The development of insecticide resistance in insect pests is a worldwide concern and elucidating the underlying mechanisms is critical for effective crop protection. Recent studies have indicated potential links between insect gut microbiota and insecticide resistance and these may apply to the diamondback moth, Plutella xylostella (L.), a globally and economically important pest of cruciferous crops. We isolated Enterococcus sp. (Firmicutes), Enterobacter sp. (Proteobacteria), and Serratia sp. (Proteobacteria) from the guts of P. xylostella and analyzed the effects on, and underlying mechanisms of insecticide resistance. Enterococcus sp. enhanced resistance to the widely used insecticide, chlorpyrifos, in P. xylostella, while in contrast, Serratia sp. decreased resistance and Enterobacter sp. and all strains of heat-killed bacteria had no effect. Importantly, the direct degradation of chlorpyrifos in vitro was consistent among the three strains of bacteria. We found that Enterococcus sp., vitamin C, and acetylsalicylic acid enhanced insecticide resistance in P. xylostella and had similar effects on expression of P. xylostella antimicrobial peptides. Expression of cecropin was down-regulated by the two compounds, while gloverin was up-regulated. Bacteria that were not associated with insecticide resistance induced contrasting gene expression profiles to Enterococcus sp. and the compounds. Our studies confirmed that gut bacteria play an important role in P. xylostella insecticide resistance, but the main mechanism is not direct detoxification of insecticides by gut bacteria. We also suggest that the influence of gut bacteria on insecticide resistance may depend on effects on the immune system. Our work advances understanding of the evolution of insecticide resistance in this key pest and highlights directions for research into insecticide resistance in other insect pest species.
Article
Full-text available
Background: Cucumber downy mildew is among the most important diseases that can disrupt cucumber production. Propamocarb, also known as propyl-[3-(dimethylamino)propyl]carbamate (PM), is a systemic carbamate fungicide pesticide that is widely applied in agricultural production because of its high efficiency of pathogens control, especially cucumber downy mildew. However, residual PM can remain in cucumbers after the disease has been controlled. To explore the molecular mechanisms of PM retention, cucumber cultivars 'D9320' (with the highest residual PM content) and 'D0351' (lowest residual PM content) were studied. High-throughput tag-sequencing (Tag-Seq) results showed that the CsDIR16 gene was related to PM residue, which was verified using transgenic technology. Results: We investigated the activity of a dirigent cucumber protein encoded by the CsDIR16 in gene response to stress induced by PM treatment. Gene-expression levels of CsDIR16 were up-regulated in the fruits, leaves, and stems of 'D0351' plants in response to PM treatment. However, in cultivar 'D9320', CsDIR16 levels were down-regulated in the leaves and stems after PM treatment, with no statistically significant differences observed in the fruits. Induction by jasmonic acid, abscisic acid, polyethylene glycol 4000, NaCl, and Corynespora cassiicola Wei (Cor) resulted in CsDIR16 up-regulation in 'D0351' and 'D9320'. Expression after salicylic acid treatment was up-regulated in 'D0351', but was down-regulated in 'D9320'. CsDIR16 overexpression lowered PM residues, and these were more rapidly reduced in CsDIR16(+) transgenic 'D9320' plants than in wild-type 'D9320' and CsDIR16(-) transgenic plants. Conclusions: Analyses of the CsDIR16-expression patterns in the cucumber cultivars with the highest and lowest levels of PM residue, and transgenic validation indicated that CsDIR16 plays a positive role in reducing PM residues. The findings of this study help understand the regulatory mechanisms occurring in response to PM stress in cucumbers and in establishing the genetic basis for developing low-pesticide residue cucumber cultivars.
Article
Full-text available
A growing body of research suggests that dysbiosis of the gut microbiota induced by environmental pollutants, such as pesticides, could have a role in the development of metabolic disorders. We have examined the long-term effects of 3 doses of the Roundup(R) herbicide (made of glyphosate and formulants) on the gut microbiota in male and female Sprague-Dawley rats. A total of 141 bacteria families were identified by a 16S sequencing analysis approach. An OPLS-DA analysis revealed an increased Bacteroidetes family S24-7 and a decreased Lactobacillaceae in 8 out of the 9 females treated with 3 different doses of R (n = 3, for each dose). These effects were confirmed by repetitive sequence-based PCR fingerprinting showing a clustering of treated females. A culture-based method showed that R had a direct effect on rat gut microbiota. Cultivable species showed different sensitivities to R, including the presence of a high tolerant or resistant strain identified as Escherichia coli by 16S rRNA sequencing. The high tolerance of this E. Coli strain was explained by the absence of the EPSPS gene (coding glyphosate target enzyme) as shown by DNA amplification. Overall, these gut microbiome disturbances showed a substantial overlap with those associated with liver dysfunction in other studies. In conclusion, we revealed that an environmental concentration of R (0.1 ppb) and other two concentrations (400 ppm and 5,000 ppm) have a sex-dependent impact on rat gut microbiome composition and thus warrants further investigation.
Article
Full-text available
MicroRNAs (miRNAs) are small endogenous noncoding single-stranded RNAs regulating gene expression in eukaryotes. They play important roles in regulating caste differentiation, behavior development, and immune defences in the honey bee, Apis mellifera (Linnaeus) (Hymenoptera: Apidae). In this study, we explored the effect of the neonicotinoid insecticide, thiamethoxam, on miRNA expression in this species using deep small RNA sequencing. The results showed that seven miRNAs were significantly differentially expressed (q-value <0.01 and |log2(fold-change)| >1) upon exposure to 10 ppb thiamethoxam over 10 d. Some candidate target genes were related to behavior, immunity, and neural function. Several miRNAs, including ame-miR-124, ame-miR-981, ame-miR-3791, and ame-miR-6038, were selected and further validated using real-time quantitative PCR analysis. The findings expand our understanding of the effects of neonicotinoid insecticides on honey bees at the molecular level.
Article
Full-text available
Recently, concerns have been raised that residues of glyphosate-based herbicides may interfere with the homeostasis of the intestinal bacterial community and thereby affect the health of humans or animals. The biochemical pathway for aromatic amino acid synthesis (Shikimate pathway), which is specifically inhibited by glyphosate, is shared by plants and numerous bacterial species. Several in vitro studies have shown that various groups of intestinal bacteria may be differently affected by glyphosate. Here, we present results from an animal exposure trial combining deep 16S rRNA gene sequencing of the bacterial community with liquid chromatography mass spectrometry (LC-MS) based metabolic profiling of aromatic amino acids and their downstream metabolites. We found that glyphosate as well as the commercial formulation Glyfonova(®)450 PLUS administered at up to fifty times the established European Acceptable Daily Intake (ADI = 0.5 mg/kg body weight) had very limited effects on bacterial community composition in Sprague Dawley rats during a two-week exposure trial. The effect of glyphosate on prototrophic bacterial growth was highly dependent on the availability of aromatic amino acids, suggesting that the observed limited effect on bacterial composition was due to the presence of sufficient amounts of aromatic amino acids in the intestinal environment. A strong correlation was observed between intestinal concentrations of glyphosate and intestinal pH, which may partly be explained by an observed reduction in acetic acid produced by the gut bacteria. We conclude that sufficient intestinal levels of aromatic amino acids provided by the diet alleviates the need for bacterial synthesis of aromatic amino acids and thus prevents an antimicrobial effect of glyphosate in vivo. It is however possible that the situation is different in cases of human malnutrition or in production animals.
Article
Full-text available
Objective To investigate the gut microbiota differences of obese children compared with the control healthy cohort to result in further understanding of the mechanism of obesity development. Methods We evaluated the 16S rRNA gene, the enterotypes, and quantity of the gut microbiota among obese children and the control cohort and learned the differences of the gut microbiota during the process of weight reduction in obese children. Results In the present study, we learned that the gut microbiota composition was significantly different between obese children and the healthy cohort. Next we found that functional changes, including the phosphotransferase system, ATP-binding cassette transporters, flagellar assembly, and bacterial chemotaxis were overrepresented, while glycan biosynthesis and metabolism were underrepresented in case samples. Moreover, we learned that the amount of Bifidobacterium and Lactobacillus increased among the obese children during the process of weight reduction. Conclusion Our results might enrich the research between gut microbiota and obesity and further provide a clinical basis for therapy for obesity. We recommend that Bifidobacterium and Lactobacillus might be used as indicators of healthy conditions among obese children, as well as a kind of prebiotic and probiotic supplement in the diet to be an auxiliary treatment for obesity.
Article
Full-text available
Introduction: Nonalcoholic steatohepatitis (NASH) is characterized by the presence of steatosis, inflammation, and ballooning degeneration of hepatocytes, with or without fibrosis. The prevalence of NASH has increased with the obesity epidemic, but its etiology is multifactorial. The current studies suggest the role of gut microbiota in the development and progression of NASH. The aim is to review the studies that investigate the relationship between gut microbiota and NASH. These review also discusses the pathophysiological mechanisms and the influence of diet on the gut-liver axis. Result: The available literature has proposed mechanisms for an association between gut microbiota and NASH, such as: modification energy homeostasis, lipopolysaccharides (LPS)-endotoxemia, increased endogenous production of ethanol, and alteration in the metabolism of bile acid and choline. There is evidence to suggest that NASH patients have a higher prevalence of bacterial overgrowth in the small intestine and changes in the composition of the gut microbiota. However, there is still a controversy regarding the microbiome profile in this population. The abundance of Bacteroidetes phylum may be increased, decreased, or unaltered in NASH patients. There is an increase in the Escherichia and Bacteroides genus. There is depletion of certain taxa, such as Prevotella and Faecalibacterium. Conclusion: Although few studies have evaluated the composition of the gut microbiota in patients with NASH, it is observed that these individuals have a distinct gut microbiota, compared to the control groups, which explains, at least in part, the genesis and progression of the disease through multiple mechanisms. Modulation of the gut microbiota through diet control offers new challenges for future studies.
Article
Full-text available
Ovarian cancer (OC) is a relatively fatal female reproductive malignancy. Since the underlying causes are uncertain, it brings us to believe that both genetic and external factors contribute toward development of this lethal disorder. Exposure to endocrine-disrupting chemicals (EDCs) in the form of occupational usage of pesticides, fungicides, herbicides, plasticizers, cosmetics, and so on is potentially carcinogenic and their ability to cause epigenetic modifications has led us to hypothesize that they may play a catalytic role in OC progression. In response to synthetic chemicals, animal models have demonstrated disturbances in the development of ovaries and steroid hormonal levels but in humans, more research is required. The present review is an attempt to address the impact of EDCs on the hormonal system and gene methylation levels that may lead to malfunctioning of the ovaries which may consequently develop in the form of cancer. It can be concluded that endocrine disruptors do have a potential carcinogenicity and their high proportions in human body may cause epigenetic modifications, prompting ovarian surface epithelium to grow in an abnormal manner.
Article
Full-text available
Pesticides are used extensively in food production to maximize crop yields. However, neonicotinoid insecticides exert unintentional toxicity to honey bees (Apis mellifera) that may partially be associated with massive population declines referred to as colony collapse disorder. We hypothesized that imidacloprid (common neonicotinoid; IMI) exposure would make Drosophila melanogaster (an insect model for the honey bee) more susceptible to bacterial pathogens, heat stress, and intestinal dysbiosis. Our results suggested that the immune deficiency (Imd) pathway is necessary for D. melanogaster survival in response to IMI toxicity. IMI exposure induced alterations in the host-microbiota as noted by increased indigenous Acetobacter and Lactobacillus spp. Furthermore, sub-lethal exposure to IMI resulted in decreased D. melanogaster survival when simultaneously exposed to bacterial infection and heat stress (37 °C). This coincided with exacerbated increases in TotA and Dpt (Imd downstream pro-survival and antimicrobial genes, respectively) expression compared to controls. Supplementation of IMI-exposed D. melanogaster with Lactobacillus plantarum ATCC 14917 mitigated survival deficits following Serratia marcescens (bacterial pathogen) septic infection. These findings support the insidious toxicity of neonicotinoid pesticides and potential for probiotic lactobacilli to reduce IMI-induced susceptibility to infection.
Book
Rachel Carson's eloquent book Silent Spring stands as one of the most important books of the twentieth century and inspired important and long-lasting changes in environmental science and government policy. This text sets Carson's study in the context of the twentieth century, reconsiders her achievement, and analyzes its legacy in light of toxic chemical use and regulation today. The book examines the history of pesticide developme