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- Inflammatory bowel disease (IBD) is a chronic inflammatory condition that affects the gastrointestinal tract, most commonly the colon and terminal ileum. IBD has a complex pathophysiology that includes both genetic and environmental factors and has two main forms: Crohn’s Disease (CD) and Ulcerative Colitis (UC). Inflammatory processes surrounding the development of IBD have been recently associated with disruptions in the gut microbiome. This review was curated from PubMed search using the terms “inflammatory bowel disease” AND “gut microbiome”. Papers were included if they discussed inflammation due to either CD or UC, and both primary and secondary research articles were utilized. Components of both the adaptive and innate immune systems have been identified responding inappropriately to the intestinal microbiome, initiating and perpetuating inflammation. T lymphocyte clones have shown cross-reactivity when in the presence of their own aerobic gut flora in patients with IBD. It has been hypothesized that since a correlation was found between elevated virulent gut microbes, high endotoxic LPS, and IBD, intestinal inflammation is possibly in part due to the suppression of regulatory T-lymphocytes and/or T-helper cell activation. Current research shows that gut dysbiosis exists in individuals with IBD. Studies have identified a decrease in the number of commensal bacterial species that benefit digestion (Faecalibacterium prausnitzii, Bifidobacterium, and Roseburia) as well as an increase in pathogenic bacterial species (Escherichia coli). Short-chain fatty acid (SCFA)-producing bacteria are reduced in patients with IBD, resulting in a decrease in the production of SCFAs, particularly butyrate. SCFAs are known to have anti-inflammatory effects. The imbalance in intestinal microbiota could explain the pathology associated with IBD, including increased epithelial permeability, dysregulated immunity, and dysfunctional metabolite production. Emerging research exploring therapies such as fecal microbiota transplantation, probiotics, and prebiotics have been seen to aid in the restoration of microbial imbalance and IBD symptoms. Metagenomic sequencing has provided a deeper understanding of the insights between the gut microbiota and their functions in the gastrointestinal tract. In conclusion, there are still research gaps in the understanding of gut microbiota and their contribution to inflammatory processes. Bridging this gap allows opportunities for strategies that contribute to treatment and prevention.
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