Instability in the composition of gut bacterial communities (dysbiosis) has been linked to common human intestinal disorders, including inflammatory bowel disease and colorectal cancer; however, it is unclear if dysbiosis can instigate disease or if it is a consequence of the underlying disorder. In this issue of the Journal of Clinical Investigation, researchers led by Mathias Chamaillard at the University Lille Nord de France in Lille, France, examined intestinal inflammation and tumorigenesis in a mouse model of dysbiosis. Dysbiosis enhanced intestinal inflammation and increased the risk for inflammation-associated colon cancer. Treatment with antibiotics or transplantation of fecal material from normal mice reduced disease risk and instigated long-term, beneficial alterations in intestinal bacteria. Conversely, transplantation of normal mice with dysbiotic fecal material increased intestinal inflammation and enhanced the risk of inflammation-associated colon cancer. These results demonstrate that gut bacterial communities play an integral role in protecting against intestinal inflammation and associated tumorigenesis.
NOD2-mediated dysbiosis predisposes mice to transmissible colitis and colorectal cancer
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