Novel insights into microbiome in colitis and colorectal cancer
- PMID: 28877044
- PMCID: PMC5826583
- DOI: 10.1097/MOG.0000000000000399
Novel insights into microbiome in colitis and colorectal cancer
Abstract
Purpose of review: Microbiota is a major player in the pathogenesis of inflammatory bowel diseases (IBD) and colorectal cancer (CRC). Here, we summarize the key advances achieved in the past 18 months (ending June 2017) toward a better understanding of the role of microbiota in colitis and CRC development.
Recent findings: Accumulating evidence shows the essential role of intestinal barrier function (e.g. mucus, IgA, LCN2, LYPD8) in protecting against bacteria-induced inflammation and tumor development. Numerous signaling pathways (e.g. TLRs and NLRs), metabolites (e.g. indole, bile acids, retinoic acid) and small noncoding RNAs (e.g. miRNA) have been identified as key mediators regulating host-microbe interactions in the intestine. Novel microbial drivers of colitis and tumorigenesis (e.g. Alistipes finegoldii, Atopobium parvalum, Peptostreptococcus anaerobius) have been identified and their disease-promoting activities have been described.
Summary: IBD-associated colorectal cancer results from a complex breakdown of communication between the host and its microbiota, involving barrier function, immune signaling and metabolites.
Conflict of interest statement
References
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- Kang M, Martin A. Microbiome and colorectal cancer: Unraveling host-microbiota interactions in colitis-associated colorectal cancer development. Semin Immunol. 2017 - PubMed
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- Morampudi V, Dalwadi U, Bhinder G, et al. The goblet cell-derived mediator RELM-beta drives spontaneous colitis in Muc2-deficient mice by promoting commensal microbial dysbiosis. Mucosal Immunol. 2016;9(5):1218–33. This study demonstrates that MUC2 deficiency in mice leads to overproduction of REGIII that predominantly targets Lactobacilli and that supplementation of Lactobacilli ameliorates spontaneous colitis MUC2-deficient mice. - PubMed
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