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.

中文翻译：

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生态失调引起的继发性胆汁酸缺乏会促进肠道炎症。

次级胆汁酸 (SBA) 源自初级胆汁酸 (PBA)，其过程依赖于少数微生物拥有的生物合成能力。为了评估 BA 在肠道炎症中的作用，我们对结肠切除术治疗的溃疡性结肠炎 (UC) 患者与对照组（家族性腺瘤性息肉病 [FAP ]）。我们表明，相对于 FAP，UC 袋降低了石胆酸和脱氧胆酸（通常是最丰富的肠道 SBA）、将 PBA 转化为 SBA 所需的基因和瘤胃球菌科（已知包括产生 SBA 的细菌的少数分类群之一） . 在三种鼠结肠炎模型中，补充 SBA 可减少肠道炎症。这种抗炎作用部分依赖于 TGR5 胆汁酸受体。这些数据表明，在易发炎的 UC 患者中，生态失调会导致 SBA 缺乏，这会促进肠道内的促炎状态，这可以通过 SBA 恢复来治疗。