期刊
CELL HOST & MICROBE
卷 27, 期 4, 页码 659-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2020.01.021
关键词
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资金
- Crohn's and Colitis Foundation Career Development Award
- KL2 Mentored Career Development Award of the Stanford Clinical Translational Science Award program to Spectrum (USA) [NIH KL2 TR 001083, NIH UL1 TR 001085]
- National Institute of Health (USA) [R01 DK101119]
- Ann and Bill Swindells Charitable Trust
- Kenneth Rainin Foundation Synergy Award (USA)
- Leslie and Douglas Ballinger (USA)
Secondary bile acids (SBAs) are derived from primary bile acids (PBAs) in a process reliant on biosynthetic capabilities possessed by few microbes. To evaluate the role of BAs in intestinal inflammation, we performed metabolomic, microbiome, metagenomic, and transcriptomic profiling of stool from ileal pouches (surgically created resevoirs) in colectomy-treated patients with ulcerative colitis (UC) versus controls (familial adenomatous polyposis [FAP]). We show that relative to FAP, UC pouches have reduced levels of lithocholic acid and deoxycholic acid (normally the most abundant gut SBAs), genes required to convert PBAs to SBAs, and Ruminococcaceae (one of few taxa known to include SBA-producing bacteria). In three murine colitis models, SBA supplementation reduces intestinal inflammation. This anti-inflammatory effect is in part dependent on the TGR5 bile acid receptor. These data suggest that dysbiosis induces SBA deficiency in inflammatory-prone UC patients, which promotes a pro-inflammatory state within the intestine that may be treated by SBA restoration.
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