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Dysbiosis of the gut microbiota in disease

There is growing evidence that dysbiosis of the gut microbiota is associated with the pathogenesis of both intestinal and extra-intestinal disorders. Intestinal disorders include inflammatory bowel disease, irritable bowel syndrome (IBS), and coeliac disease, while extra-intestinal disorders include...

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Autores principales: Carding, Simon, Verbeke, Kristin, Vipond, Daniel T., Corfe, Bernard M., Owen, Lauren J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Co-Action Publishing 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315779/
https://www.ncbi.nlm.nih.gov/pubmed/25651997
http://dx.doi.org/10.3402/mehd.v26.26191
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author Carding, Simon
Verbeke, Kristin
Vipond, Daniel T.
Corfe, Bernard M.
Owen, Lauren J.
author_facet Carding, Simon
Verbeke, Kristin
Vipond, Daniel T.
Corfe, Bernard M.
Owen, Lauren J.
author_sort Carding, Simon
collection PubMed
description There is growing evidence that dysbiosis of the gut microbiota is associated with the pathogenesis of both intestinal and extra-intestinal disorders. Intestinal disorders include inflammatory bowel disease, irritable bowel syndrome (IBS), and coeliac disease, while extra-intestinal disorders include allergy, asthma, metabolic syndrome, cardiovascular disease, and obesity. In many of these conditions, the mechanisms leading to disease development involves the pivotal mutualistic relationship between the colonic microbiota, their metabolic products, and the host immune system. The establishment of a ‘healthy’ relationship early in life appears to be critical to maintaining intestinal homeostasis. Whilst we do not yet have a clear understanding of what constitutes a ‘healthy’ colonic microbiota, a picture is emerging from many recent studies identifying particular bacterial species associated with a healthy microbiota. In particular, the bacterial species residing within the mucus layer of the colon, either through direct contact with host cells, or through indirect communication via bacterial metabolites, may influence whether host cellular homeostasis is maintained or whether inflammatory mechanisms are triggered. In addition to inflammation, there is some evidence that perturbations in the gut microbiota is involved with the development of colorectal cancer. In this case, dysbiosis may not be the most important factor, rather the products of interaction between diet and the microbiome. High-protein diets are thought to result in the production of carcinogenic metabolites from the colonic microbiota that may result in the induction of neoplasia in the colonic epithelium. Ever more sensitive metabolomics methodologies reveal a suite of small molecules produced in the microbiome which mimic or act as neurosignallers or neurotransmitters. Coupled with evidence that probiotic interventions may alter psychological endpoints in both humans and in rodent models, these data suggest that CNS-related co-morbidities frequently associated with GI disease may originate in the intestine as a result of microbial dysbiosis. This review outlines the current evidence showing the extent to which the gut microbiota contributes to the development of disease. Based on evidence to date, we can assess the potential to positively modulate the composition of the colonic microbiota and ameliorate disease activity through bacterial intervention.
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spelling pubmed-43157792015-02-23 Dysbiosis of the gut microbiota in disease Carding, Simon Verbeke, Kristin Vipond, Daniel T. Corfe, Bernard M. Owen, Lauren J. Microb Ecol Health Dis Engihr Supplement There is growing evidence that dysbiosis of the gut microbiota is associated with the pathogenesis of both intestinal and extra-intestinal disorders. Intestinal disorders include inflammatory bowel disease, irritable bowel syndrome (IBS), and coeliac disease, while extra-intestinal disorders include allergy, asthma, metabolic syndrome, cardiovascular disease, and obesity. In many of these conditions, the mechanisms leading to disease development involves the pivotal mutualistic relationship between the colonic microbiota, their metabolic products, and the host immune system. The establishment of a ‘healthy’ relationship early in life appears to be critical to maintaining intestinal homeostasis. Whilst we do not yet have a clear understanding of what constitutes a ‘healthy’ colonic microbiota, a picture is emerging from many recent studies identifying particular bacterial species associated with a healthy microbiota. In particular, the bacterial species residing within the mucus layer of the colon, either through direct contact with host cells, or through indirect communication via bacterial metabolites, may influence whether host cellular homeostasis is maintained or whether inflammatory mechanisms are triggered. In addition to inflammation, there is some evidence that perturbations in the gut microbiota is involved with the development of colorectal cancer. In this case, dysbiosis may not be the most important factor, rather the products of interaction between diet and the microbiome. High-protein diets are thought to result in the production of carcinogenic metabolites from the colonic microbiota that may result in the induction of neoplasia in the colonic epithelium. Ever more sensitive metabolomics methodologies reveal a suite of small molecules produced in the microbiome which mimic or act as neurosignallers or neurotransmitters. Coupled with evidence that probiotic interventions may alter psychological endpoints in both humans and in rodent models, these data suggest that CNS-related co-morbidities frequently associated with GI disease may originate in the intestine as a result of microbial dysbiosis. This review outlines the current evidence showing the extent to which the gut microbiota contributes to the development of disease. Based on evidence to date, we can assess the potential to positively modulate the composition of the colonic microbiota and ameliorate disease activity through bacterial intervention. Co-Action Publishing 2015-02-02 /pmc/articles/PMC4315779/ /pubmed/25651997 http://dx.doi.org/10.3402/mehd.v26.26191 Text en © 2015 Simon Carding et al. http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Engihr Supplement
Carding, Simon
Verbeke, Kristin
Vipond, Daniel T.
Corfe, Bernard M.
Owen, Lauren J.
Dysbiosis of the gut microbiota in disease
title Dysbiosis of the gut microbiota in disease
title_full Dysbiosis of the gut microbiota in disease
title_fullStr Dysbiosis of the gut microbiota in disease
title_full_unstemmed Dysbiosis of the gut microbiota in disease
title_short Dysbiosis of the gut microbiota in disease
title_sort dysbiosis of the gut microbiota in disease
topic Engihr Supplement
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315779/
https://www.ncbi.nlm.nih.gov/pubmed/25651997
http://dx.doi.org/10.3402/mehd.v26.26191
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