应用领域

Dysbiosis-Induced Secondary Bile Acid Deficiency Promotes Intestinal Inflammation

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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基因水平：PCR Array、RT-PCR、PCR、单细胞测序
蛋白水平：MSD、Luminex、CBA、Elispot、Antibody Array、ELISA、Sengenics
细胞水平：细胞染色、细胞分选、细胞培养、细胞功能
组织水平：空间多组学、多重荧光免疫组化、免疫组化、免疫荧光
数据分析：流式数据分析、组化数据分析、多因子数据分析

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