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Involvement of Ffar2 in the reduction of NPP‐induced IL‐6 by inoculation of LCC onto S. epidermidis‐colonized mice (A) S. epidermidis‐colonized ICR mice were intranasally applied with LCC (+LCC) or PBS (‐LCC) 1 h before inoculation of NPP for 6 h. The level of IL‐6 in BALF induced by NPP was expressed as fold change over that induced by PBS. (B) S. epidermidis‐colonized ICR mice were given GLPG‐0974, a Ffar2 antagonist (+), or vehicle (ethanol) alone (‐) by gastric gavage every day for 3 days. After administration of GLPG‐0974, mice were intranasally applied with LCC six hours before inoculation with NPP. The level of IL‐6 in BALF of mice given with GLPG‐0974 was expressed as fold change over that in BALF of mice given without GLPG‐0974. The P‐value of < 0.001 (**); < 0.0001 (***) from three independent experiments with mean ± SD is shown.
Source publication
Infection by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) can trigger excessive interleukin (IL)‐6 signalling, leading to a myriad of biological effects including a cytokine storm that contributes to multiple organ failure in severe coronavirus disease 2019 (COVID‐19). Using a mouse model, we demonstrated that nasal inoculation of n...
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Introduction
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Citations
... Shifting focus to COVID-19, the cytokine storm observed in this disease is triggered by the release of interleukin-6 (IL-6) from alveolar macrophages [34]. Interestingly, FFAR2 appears to play a role in regulating probiotic activity, which has been shown to reduce IL-6 levels in COVID-19 patients [35,36]. ...
... FFAR2 can modulate inflammation through both immune cell activation [31] and gut microbiota interactions [32]. Some studies suggest it can decrease the inflammatory marker IL-6 by regulating beneficial gut bacteria (probiotics) [35,36]. Our findings demonstrate higher normalized FFAR2 expression in MAFLD patients compared to controls, with similar observations in patients with type 2 diabetes mellitus (T2DM). ...
Metabolic-associated fatty liver disease (MAFLD) is a risk factor for severe COVID-19. This study explores the potential influence of gut hormone receptor and immune response gene expression on COVID-19 outcomes in MAFLD patients. Methods: We investigated gene expression levels of AHR, FFAR2, FXR, and TGR5 in patients with MAFLD and COVID-19 compared to controls. We examined associations between gene expression and clinical outcomes. Results: COVID-19 patients displayed altered AHR expression, potentially impacting immune response and recovery. Downregulated AHR in patients with MAFLD correlated with increased coagulation parameters. Elevated FFAR2 expression in patients with MAFLD was linked to specific immune cell populations and hospital stay duration. A significantly lower FXR expression was observed in both MAFLD and severe COVID-19. Conclusion: Our findings suggest potential modulatory roles for AHR, FFAR2, and FXR in COVID-19 and MAFLD.
... Probiotic-based experimental treatments for other nasal persistent conditions such as rhinitis are under investigation (Sarfraz et al., 2024), and the airway probiotic activity of other bacterial components of the human nasal microbiome is being explored. This is the case for nasal Staphylococcus epidermidis, whose protective role against influenza and SARS-CoV-2 viral infections has been shown, as it fermentates carbonrich molecules yielding short-chain fatty acids and electricity, which have anti-inflammatory properties and influence bacterial nasal colonization, respectively (Kao et al., 2022). In this context, direct topical probiotic use in the respiratory tract could also be considered as a targeted treatment option for chronic lung disease patients. ...
The human respiratory system is constantly exposed to environmental stimuli, sometimes including toxicants, which can trigger dysregulated lung immune responses that lead to respiratory symptoms, impaired lung function and airway diseases. Evidence supports that the microbiome in the lungs has an indispensable role in respiratory health and disease, acting as a local gatekeeper that mediates the interaction between the environmental cues and respiratory health. Moreover, the microbiome in the lungs is intimately intertwined with the oral microbiome through the oral–lung axis. Here, we discuss the intricate three‐way relationship between (i) cigarette smoking, which has strong effects on the microbial community structure of the lung; (ii) microbiome dysbiosis and disease in the oral cavity; and (iii) microbiome dysbiosis in the lung and its causal role in patients suffering chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. We highlight exciting outcomes arising from recently established interactions in the airway between environmental exposures, microbiome, metabolites–functional attributes and the host, as well as how these associations have the potential to predict the respiratory health status of the host through an airway microbiome health index. For completion, we argue that incorporating (synthetic) microbial community ecology in our contemporary understanding of lung disease presents challenges and also rises novel opportunities to exploit the oral–lung axis and its microbiome towards innovative airway disease diagnostics, prognostics, patient stratification and microbiota‐targeted clinical interventions in the context of current therapies.
... Shifting focus to COVID-19, the cytokine storm observed in this disease is triggered by the release of interleukin-6 (IL-6) from alveolar macrophages [27]. Interestingly, FFAR2 appears to play a role in regulating probiotic activity, which has been shown to reduce IL-6 levels in COVID-19 patients [28,29]. ...
... FFAR2 can modulate inflammation through both immune cell activation [24] and gut microbiota interactions [25]. Some studies suggest it can decrease the inflammatory marker IL-6 by regulating beneficial gut bacteria (probiotics) [28,29]. Our findings demonstrate higher normalized FFAR2 expression in MAFLD patients compared to controls, with similar observations in patients with type 2 diabetes mellitus (T2DM). ...
Metabolic-associated fatty liver disease (MAFLD) is a risk factor for severe COVID-19. This study explores the potential influence of gut hormone receptor and immune response gene expression on COVID-19 outcomes in MAFLD patients. Methods: We investigated gene expression levels of AHR, FFAR2, FXR, and TGR5 in patients with MAFLD and COVID-19 compared to controls. We examined associations between gene expression and clinical outcomes. Results: COVID-19 patients displayed altered AHR expression, potentially impacting immune response and recovery. Downregulated AHR in MAFLD patients correlated with increased coagulation parameters. Elevated FFAR2 expression in MAFLD linked to specific immune cell populations and hospital stay duration. Significantly lower FXR expression was observed in both MAFLD and severe COVID-19. Conclusion: Our findings suggest potential modulatory roles for AHR, FFAR2, and FXR in COVID-19 and MAFLD.
Keywords: COVID-19; MAFLD; AHR; FXR; Gene expression
... Finally, administering SARS-CoV-2 N protein to mice intratracheally causes acute lung injury while nasal inoculation with SARS-CoV-2 N protein increases levels of IL-6 in the lungs. Complement activation and signaling pathways activated through Toll-like receptor 2 may contribute to these outcomes [144,147]. In fact, the NF-κB p65 phosphorylation is linked to lung damage. ...
... Pretreatment with a riboflavin kinase inhibitor (i.e., roseoflavin) can reduce the electricity production in Gram-positive bacteria [29]. In this study, we showed that a 24 h pretreatment of L. plantarum MA with roseoflavin significantly reduced the concentration Pretreatment with a riboflavin kinase inhibitor (i.e., roseoflavin) can reduce the electricity production in Gram-positive bacteria [29]. ...
... Pretreatment with a riboflavin kinase inhibitor (i.e., roseoflavin) can reduce the electricity production in Gram-positive bacteria [29]. In this study, we showed that a 24 h pretreatment of L. plantarum MA with roseoflavin significantly reduced the concentration Pretreatment with a riboflavin kinase inhibitor (i.e., roseoflavin) can reduce the electricity production in Gram-positive bacteria [29]. In this study, we showed that a 24 h pretreatment of L. plantarum MA with roseoflavin significantly reduced the concentration of FMN by approximately 12 folds (Figure 3b) while also decreasing electricity production (Figure 3c), suggesting that the bioelectrical activity of L. plantarum MA was mediated through the FMN-based EET system. ...
The mechanism behind how flavin mononucleotide (FMN)-producing bacteria attach to a host intestine remains unclear. In order to address this issue, this study isolated the Gram-positive bacteria Lactobacillus plantarum from Mongolian fermented Airag, named L. plantarum MA. These bacteria were further employed as the model microbes, and their electrogenic properties were first identified by their significant expression of type II NADH-quinone oxidoreductase. This study also demonstrated that the electrical activity of L. plantarum MA can be conducted through flavin mononucleotide (FMN)-based extracellular electron transfer, which is highly dependent on the presence of a carbon source in the medium. Our data show that approximately 15 µM of FMN, one of the key electron donors for the generation of electricity, can be produced from L. plantarum MA, as they were cultured in the presence of lactulose for 24 h. We further demonstrated that the electrical activity of L. plantarum MA can promote microbial adhesion and can thus enhance the colonization effectiveness of Caco-2 cells and mouse cecum. Such enhanced adhesiveness was attributed to the increased expression of type I collagens in the intestinal epithelium after treatment with L. plantarum MA. This study reveals the mechanism behind the electrogenic activity of L. plantarum MA and shows how the bacteria utilize electricity to modulate the protein expression of gut tissue for an enhanced adhesion process.
... SARS-CoV-2 N-protein also up-regulates the expression of tissue factor and intracellular adhesion molecule 1, markers involved in vascular coagulation and inflammation, and glucose transporter 4, a diabetic marker [27]. Lastly, complement activation and the activation of signaling pathways through Toll-like receptor 2 might be involved in increasing levels of IL-6 in the lungs of mice inoculated nasally with SARS-CoV-2 N-protein and inducing acute lung injury in mice administrated intratracheally with SARS-CoV-2 N-protein [26,28]. Indeed, the lung injury is associated with NF-κB p65 phosphorylation. ...
The coronavirus disease 2019 (COVID-19) has caused enormous health risks and global economic disruption. This disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The SARS-CoV-2 nucleocapsid protein is a structural protein involved in viral replication and assembly. There is accumulating evidence indicating that the nucleocapsid protein is multi-functional, playing a key role in the pathogenesis of COVID-19 and antiviral immunity against SARS-CoV-2. Here, we summarize its potential application in the prevention of COVID-19, which is based on its role in inflammation, cell death, antiviral innate immunity, and antiviral adapted immunity.
Aim:
Certain probiotic bacteria have been shown to possess an immunomodulatory effect and a protective effect on influenza infections. Using the Staphylococcus epidermidis K1 (S. epidermidis K1)-colonized mice model, we assessed the effect of nasal administration of glycerol or flavin mononucleotide (FMN) on the production of interleukin (IL)-6 mediated by the severe acute respiratory syndrome coronavirus 2 (SARS2-CoV) nucleocapsid protein (NPP).
Methods and results:
FMN, one of the key electron donors for the generation of electricity facilitated by S. epidermidis ATCC 12228, was detected in the glycerol fermentation medium. Compared to S. epidermidis ATCC 12228, the S. epidermidis K1 isolate showed significant expression of the electron transfer genes, including pyruvate dehydrogenase (pdh), riboflavin kinase (rk), 1,4-dihydroxy-2-naphthoate octaprenyltransferase (menA), and type II NADH: quinone oxidoreductase (ndh2). ICR mice were intranasally administered with S. epidermidis K1 with or without pre-treatment with riboflavin kinase inhibitors, then nasally treated with glycerol or FMN before inoculating the NPP. Furthermore, J774A.1 macrophages were exposed to NPP serum and then treated with NPP of SARS2-CoV. The IL-6 levels in the bronchoalveolar lavage fluid (BALF) of mice and macrophages were quantified using a mouse IL-6 enzyme-linked immunosorbent assay (ELISA) kit.
Conclusions:
Here, we report that nasal administration of NPP strongly elevates IL-6 levels in both BALF and J774A.1 macrophages. It is worth noting that NPP-neutralizing antibodies can decrease IL-6 levels in macrophages. The nasal administration of glycerol or FMN to S. epidermidis K1-colonized mice results in a reduction of NPP-induced IL-6 production.
Background
Acute myocardial infarction (AMI) is one of the leading causes of death worldwide. The etiology of AMI is complex and has not been fully defined. In recent years, the role of immune response in the development, progression and prognosis of AMI has received increasing attention. The aim of this study was to identify key genes associated with the immune response in AMI and to analyze their immune infiltration.
Methods
The study included a total of two GEO databases, containing 83 patients with AMI and 54 healthy individuals. We used the linear model of microarray data (limma) package to find the differentially expressed genes associated with AMI, performing weighted gene co-expression analysis (WGCNA) to further identify the genes associated with inflammatory response to AMI. We found the final hub genes through the protein-protein interaction (PPI) network and least absolute shrinkage and selection operator (LASSO) regression model. To verify the above conclusions, we constructed mice AMI model, extracting myocardial tissue to perform qRT-PCR. Furthermore, the CIBERSORT tool for immune cells infiltration analysis was also carried out.
Results
A total of 5,425 significant up-regulated and 2,126 down-regulated genes were found in GSE66360 and GSE24519 . A total of 116 immune-related genes in close association with AMI were screened by WGCNA analysis. These genes were mostly clustered in the immune response on the basis of GO and KEGG enrichment. With construction of PPI network and LASSO regression analysis, this research found three hub genes (SOCS2, FFAR2, MYO10) among these differentially expressed genes. The immune cell infiltration results revealed that significant differences could be found on T cells CD4 memory activated, Tregs (regulatory T cells), macrophages M2, neutrophils, T cells CD8, T cells CD4 naive, eosinophils between controls and AMI patients.
Extracellular electron transfer (EET) is a bioelectrochemical process performed by electrochemically active bacteria (EAB) found in host-associated environments, including plant and animal ecosystems and fermenting plant- and animal-derived foods. Through direct or mediated electron transfer pathways, certain bacteria use EET to enhance ecological fitness with host-impacting effects. In the plant rhizosphere, electron acceptors support the growth of EAB such as members of the Geobacter, cable bacteria, and some clostridia with the capacity to influence iron and heavy metal uptake by plants. In animal microbiomes, EET is associated with diet-derived iron in the intestines of soil-dwelling termites, earthworms, and beetle larvae. EET is also associated with the colonization and metabolism of some bacteria in human and animal microbiomes, such as Streptococcus mutans in the mouth, Enterococcus faecalis and Listeria monocytogenes in the intestine, and Pseudomonas aeruginosa in the lungs. During the fermentation of plant tissues and bovine milk, lactic acid bacteria like Lactiplantibacillus plantarum and Lactococcus lactis may use EET to increase their growth and food acidification, as well as decrease environmental oxidation-reduction potential. EET is thus likely an important metabolic pathway for host-associated bacteria and has implications for ecosystem function, health and disease, and biotechnological applications.
