Bile acid–induced metabolic changes in the colon promote Enterobacteriaceae expansion and associate with dysbiosis in Crohn’s disease

肠杆菌科 回肠 炎症性肠病 微生物学 失调 生物 肠粘膜 肠道菌群 内科学 免疫学 医学 疾病 大肠杆菌 内分泌学 生物化学 基因
作者
Ravi Holani,Haggai Bar‐Yoseph,Zakhar Krekhno,Antonio Serapio-Palacios,Kyung‐Mee Moon,R. Greg Stacey,Katherine Donald,Wanyin Deng,Brian Bressler,Armando Alcázar Magaña,Leonard J. Foster,Michael G. Atser,James D. Johnson,B. Brett Finlay
出处
期刊:Science Signaling [American Association for the Advancement of Science (AAAS)]
卷期号:17 (867)
标识
DOI:10.1126/scisignal.adl1786
摘要

Bile acids (BAs) affect the growth of potentially pathogenic commensals, including those from the Enterobacteriaceae family, which are frequently overrepresented in inflammatory bowel disease (IBD). BAs are normally reabsorbed in the ileum for recycling and are often increased in the colonic lumina of patients with IBD, including those with Crohn's disease (CD). Here, we investigated the influence of BAs on gut colonization by Enterobacteriaceae. We found increased abundance of Enterobacteriaceae in the colonic mucosae of patients with CD with a concomitant decrease in the transporters that resorb BAs in the ileum. The increase in Enterobacteriaceae colonization was greater in the colons of patients who had undergone terminal ileum resection compared with those with intact ileum, leading us to hypothesize that BAs promote intestinal colonization by Enterobacteriaceae. Exposure of human colonic epithelial cell lines to BAs reduced mitochondrial respiration, increased oxygen availability, and enhanced the epithelial adherence of several Enterobacteriaceae members. In a publicly available human dataset, mucosal Enterobacteriaceae was negatively associated with the expression of genes related to mitochondrial function. In a murine model, increased intestinal BA availability enhanced colonization by
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