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논문 기본 정보

자료유형
학술저널
저자정보
Hiroko Nagao-Kitamoto (University of Michigan Medical School) Nobuhiko Kamada (University of Michigan Medical School)
저널정보
대한면역학회 Immune Network Immune Network Vol.17 No.1
발행연도
2017.2
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1 - 12 (12page)

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초록· 키워드

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A vast community of commensal microorganisms, commonly referred to as the gut microbiota, colonizes the gastrointestinal tract (GI). The involvement of the gut microbiota in the maintenance of the gut ecosystem is two-fold: it educates host immune cells and protects the host from pathogens. However, when healthy microbial composition and function are disrupted (dysbiosis), the dysbiotic gut microbiota can trigger the initiation and development of various GI diseases, including inflammatory bowel disease (IBD). IBD, primarily includes ulcerative colitis (UC) and Crohn"s disease (CD), is a major global public health problem affecting over 1 million patients in the United States alone. Accumulating evidence suggests that various environmental and genetic factors contribute to the pathogenesis of IBD. In particular, the gut microbiota is a key factor associated with the triggering and presentation of disease. Gut dysbiosis in patients with IBD is defined as a reduction of beneficial commensal bacteria and an enrichment of potentially harmful commensal bacteria (pathobionts). However, as of now it is largely unknown whether gut dysbiosis is a cause or a consequence of IBD. Recent technological advances have made it possible to address this question and investigate the functional impact of dysbiotic microbiota on IBD. In this review, we will discuss the recent advances in the field, focusing on host-microbial cross-talk in IBD.

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INTRODUCTION
IBD-associated dysbiosis in the gut
The utility of a humanized gnotobiotic mouse system
Discussion
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UCI(KEPA) : I410-ECN-0101-2017-517-002233559