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자료유형
학술저널
저자정보
Hiroko Nagao-Kitamoto (Department of Internal Medicine University of Michigan Medical School Ann Arbor Michigan USA) Sho Kitamoto (Department of Internal Medicine University of Michigan Medical School Ann Arbor Michigan USA) Peter Kuffa (Department of Internal Medicine University of Michigan Medical School Ann Arbor Michigan USA) Nobuhiko Kamada (Department of Internal Medicine University of Michigan Medical School Ann Arbor Michigan USA)
저널정보
대한장연구학회 Intestinal research Intestinal research Vol.14 No.2
발행연도
2016.1
수록면
127 - 138 (12page)

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The gastrointestinal (GI) tract is colonized by a dense community of commensal microorganisms referred to as the gut microbiota. The gut microbiota and the host have co-evolved, and they engage in a myriad of immunogenic and metabolic interactions. The gut microbiota contributes to the maintenance of host health. However, when healthy microbial structure is perturbed,a condition termed dysbiosis, the altered gut microbiota can trigger the development of various GI diseases includinginflammatory bowel disease, colon cancer, celiac disease, and irritable bowel syndrome. There is a growing body of evidencesuggesting that multiple intrinsic and extrinsic factors, such as genetic variations, diet, stress, and medication, can dramaticallyaffect the balance of the gut microbiota. Therefore, these factors regulate the development and progression of GI diseases byinducing dysbiosis. Herein, we will review the recent advances in the field, focusing on the mechanisms through which intrinsicand extrinsic factors induce dysbiosis and the role a dysbiotic microbiota plays in the pathogenesis of GI diseases.

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