Dysbiosis of the gut microbiota in disease

Carding, Simon, Verbeke, Kristin, Vipond, Daniel T., Corfe, Bernard M and Owen, Lauren J. (2015) Dysbiosis of the gut microbiota in disease. Microbial Ecology, 26. pp. 26191-26200. ISSN 0095-3628

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    Abstract

    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 (IBD), irritable bowel syndrome (IBS) and celiac 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.

    Item Type: Article
    Additional Information: © 2015 Simon Carding et al. This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License (http://creativecommons.org/licenses/by-nc/3.0/), permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
    Uncontrolled Keywords: microbiome,short-chain fatty acids,gut health,colonic metabolome,gut-brain-axis,inflammation
    Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
    Depositing User: Pure Connector
    Date Deposited: 14 Apr 2016 14:00
    Last Modified: 08 Oct 2017 06:09
    URI: https://ueaeprints.uea.ac.uk/id/eprint/58245
    DOI:

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