Dysbiosis of the gut microbiota in disease
By Simon R. Carding, K. Verbeke, Daniel T. Vipond, B. Corfe, Lauren Owen. Microbial Ecology in Health and Disease, 2015
1,618 citations recorded by the source corpus.
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.
Subfields: Gastroenterology, Infectious Diseases, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/f77d539d2904ecc8bc9ceb9019dc0e502f1489eb
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Citations in the corpus
- The Firmicutes/Bacteroidetes Ratio: A Relevant Marker of Gut Dysbiosis in Obese Patients? (2020, background): “Gut dysbiosis is also associated with various pathologic conditions affecting the gastrointestinal tract (diarrhea, irritable bowel syndrome) [4], the immune system (allergy, multiple sclerosis, type 1 diabetes, inflammatory bowel diseases, rheumatoid arthritis) [4–6], the central nervous system (Al”
- Mucosal microbiome dysbiosis in gastric carcinogenesis (2017, background): “33 The overall knowledge on the roles of gastric microbes apart from H. pylori in GC is still limited, despite evidences of potential roles of non-H. pylori bacteria in GC.”
- Long COVID or Post-acute Sequelae of COVID-19 (PASC): An Overview of Biological Factors That May Contribute to Persistent Symptoms (2021, background): “However, across the globe, a subset of patients who sustain an acute SARS CoV-2 infection are developing a wide range of persistent symptoms that do not resolve over the course of many months (Carfì et al., 2020; Davis et al., 2020; Huang C. et al., 2021) (Figure 1).”