Community Health Care: Therapeutic Opportunities in the Human Microbiome

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Science translational medicine (Impact Factor: 15.84). 04/2011; 3(78):78ps12. DOI: 10.1126/scitranslmed.3001626
Source: PubMed


We are never alone. Humans coexist with diverse microbial species that live within and upon us--our so-called microbiota. It is now clear that this microbial community is essentially another organ that plays a fundamental role in human physiology and disease. Basic and translational research efforts have begun to focus on deciphering mechanisms of microbiome function--and learning how to manipulate it to benefit human health. In this Perspective, we discuss therapeutic opportunities in the human microbiome.

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    • "Most of the results published so far are from individuals living on food based on a few carbohydrates (wheat, rice, corn, and potatoes). The need for studies in larger groups of individuals followed over longer periods of time is obvious, as well as the need for data from cohorts living on other sources of carbohydrates (82, 83); more information is also needed about microbiota in various intestinal compartments. In addition, accepting the lifelong cross-talks that take place between a host and its microbiota and the adaptability of the microflora to local or regional food, we should start thinking about the sustainability of intestinal microbiota in cohorts of people not living on a ‘Westernized diet’, and attempts should be made to investigate or at least save feces from groups of people living on such food. "
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    ABSTRACT: It is now generally accepted that the 'central genome dogma' (i.e. a causal chain going from DNA to RNA to proteins and downstream to biological functions) should be replaced by the 'fluid genome dogma', that is, complex feed-forward and feed-back cycles that interconnect organism and environment by epigenomic programing - and reprograming - throughout life and at all levels, sometimes also down the generations. The epigenomic programing is the net sum of interactions derived from own metabolism and microbiota as well as external factors such as diet, pharmaceuticals, environmental compounds, and so on. It is a growing body of results indicating that many chronic metabolic and degenerative disorders and diseases - often called 'civilization diseases' - are initiated and/or influenced upon by non-optimal epigenomic programing, often taking place early in life. In this context, the first 1,000 days of life - from conception into early infancy - is often called the most important period of life. The following sections present some major mechanisms for epigenomic programing as well as some factors assumed to be of importance. The need for more information about own genome and metagenome, as well as a substantial lack of adequate information regarding dietary and environmental databases are also commented upon. However, the mere fact that we can influence epigenomic health programing opens up the way for prophylactic and therapeutic interventions. The authors underline the importance of creating a 'Human Gut Microbiota and Epigenomic Platform' in order to facilitate interdisciplinary collaborations among scientists and clinicians engaged in host microbial ecology, nutrition, metagenomics, epigenomics and metabolomics as well as in disease epidemiology, prevention and treatment.
    Microbial Ecology in Health and Disease 05/2014; 25. DOI:10.3402/mehd.v25.24145
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    • "Furthermore, because living probiotic bacteria can colonize the intestinal tract for a long period of time and produce carcinogenic acetaldehyde locally, potentially they can be more dangerous than traditional dairy lactic acid bacteria because of increased total exposure to this bacterial metabolite (53, 54). Some scientists consider that ‘genetic engineering of the human microbiota will enable to endow its members with new desirable functions that treat diseases or promote health’ (10). In spite of the scientific attractiveness of this idea, from a prolonged point of view, the massed introduction of genetic engineering live probiotic microbes in practice may have extremely dangerous ecological and medical consequences even when using such novel platform of microbial cells design as synthetic biology approaches. "
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    ABSTRACT: Traditionally, probiotics on the base of live microorganisms are considered to be both beneficial and safe. Unfortunately, their effects may have short-term success or are absent or uncertain. Some symbiotic (probiotic) microorganisms with known beneficial health affects may cause opportunistic infections, increase incidence of allergic sensitization and autoimmune disorders, produce microecological imbalance, modify gene expression, transfer antibiotic resistant and virulence genes, cause disorders in epigenome and genome integrity, induce chromosomal DNA damage, and activate signaling pathways associated with cancer and other chronic diseases. The commercially available probiotics should be considered as a first generation means of correcting microecological disorders. Further, their development will include the selection of natural metabiotics and/or working out the synthetic (or semi-synthetic) metabiotics that will be analogies or improved copies of natural bioactives, produced by symbiotic (probiotic) microorganisms. Metabiotics are the structural components of probiotic microorganisms and/or their metabolites and/or signaling molecules with a determined (known) chemical structure that can optimize host-specific physiological functions, regulator, metabolic and/or behavior reactions connected with the activity of host indigenous microbiota. Metabiotics have some advantages because of their exact chemical structure, well dosed, very safe and long shelf-life. Thus, now metabiotics should not consider myth; they are the result of the natural evolution of probiotic conception.
    Microbial Ecology in Health and Disease 04/2013; 24. DOI:10.3402/mehd.v24i0.20399
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    • "However, the absorption of intact gliadin-reactive peptides along the gastrointestinal tract may vary between individuals. Diversity in the gut microflora (microbiome) and in the accompanying diet could have a dramatic impact on the resultant peptide concentration in feces (20). Although a low digestion rate of gluten peptides would reduce their absorption, most of the undigested gluten peptides would be excreted, and either rapid immunochromatographic strips or ELISAs could be used to detect gluten ingestion in feces. "
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    ABSTRACT: Certain immunotoxic peptides from gluten are resistant to gastrointestinal digestion and can interact with celiac-patient factors to trigger an immunologic response. A gluten-free diet (GFD) is the only effective treatment for celiac disease (CD), and its compliance should be monitored to avoid cumulative damage. However, practical methods to monitor diet compliance and to detect the origin of an outbreak of celiac clinical symptoms are not available. We assessed the capacity to determine the gluten ingestion and monitor GFD compliance in celiac patients by the detection of gluten and gliadin 33-mer equivalent peptidic epitopes (33EPs) in human feces. Fecal samples were obtained from healthy subjects, celiac patients, and subjects with other intestinal pathologies with different diet conditions. Gluten and 33EPs were analyzed by using immunochromatography and competitive ELISA with a highly sensitive antigliadin 33-mer monoclonal antibody. The resistance of a significant part of 33EPs to gastrointestinal digestion was shown in vitro and in vivo. We were able to detect gluten peptides in feces of healthy individuals after consumption of a normal gluten-containing diet, after consumption of a GFD combined with controlled ingestion of a fixed amount of gluten, and after ingestion of <100 mg gluten/d. These methods also allowed us to detect GFD infringement in CD patients. Gluten-derived peptides could be sensitively detected in human feces in positive correlation with the amount of gluten intake. These techniques may serve to show GFD compliance or infringement and be used in clinical research in strategies to eliminate gluten immunotoxic peptides during digestion. This trial was registered at as NCT01478867.
    American Journal of Clinical Nutrition 03/2012; 95(3):670-7. DOI:10.3945/ajcn.111.026708 · 6.77 Impact Factor
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