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      Gut microbiota in the pathogenesis of inflammatory bowel disease.

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          Abstract

          Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a chronic and relapsing inflammatory disorder of the intestine. Although its incidence is increasing globally, the precise etiology remains unclear and a cure for IBD has yet to be discovered. The most accepted hypothesis of IBD pathogenesis is that complex interactions between genetics, environmental factors, and the host immune system lead to aberrant immune responses and chronic intestinal inflammation. The human gut harbors a complex and abundant aggregation of microbes, collectively referred to as the gut microbiota. The gut microbiota has physiological functions associated with nutrition, the immune system, and defense of the host. Recent advances in next-generation sequencing technology have identified alteration of the composition and function of the gut microbiota, which is referred to as dysbiosis, in IBD. Clinical and experimental data suggest dysbiosis may play a pivotal role in the pathogenesis of IBD. This review is focused on the physiological function of the gut microbiota and the association between the gut microbiota and pathogenesis in IBD. In addition, we review the therapeutic options for manipulating the altered gut microbiota, such as probiotics and fecal microbiota transplantation.

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          Author and article information

          Journal
          Clin J Gastroenterol
          Clinical journal of gastroenterology
          Springer Nature
          1865-7265
          1865-7265
          Feb 2018
          : 11
          : 1
          Affiliations
          [1 ] Department of Medicine, Shiga University of Medical Science, Seta-Tsukinowa, Otsu, 520-2192, Japan. atsuda@belle.shiga-med.ac.jp.
          [2 ] Laboratory of Animal Science, Department of Agriculture and Life Science, Kyoto Prefectural University, Kyoto, 606-8522, Japan.
          [3 ] Department of Medicine, Shiga University of Medical Science, Seta-Tsukinowa, Otsu, 520-2192, Japan.
          [4 ] Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan.
          Article
          10.1007/s12328-017-0813-5
          10.1007/s12328-017-0813-5
          29285689

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