肠易激综合征
鹅去氧胆酸
腹泻
胃肠病学
G蛋白偶联胆汁酸受体
胆汁酸
拟杆菌
内科学
医学
肠道菌群
脆弱类杆菌
发病机制
肠-脑轴
粪便
生物
微生物学
细菌
免疫学
抗生素
遗传学
作者
Kai Zhan,Haomeng Wu,Yongyin Xu,Kehan Rao,Huan Zheng,Shumin Qin,Yuanming Yang,Jia Rui,Weihuan Chen,Shaogang Huang
出处
期刊:MSystems
[American Society for Microbiology]
日期:2024-02-08
被引量:3
标识
DOI:10.1128/msystems.01299-23
摘要
Visceral hypersensitivity and intestinal mucosal barrier damage are important factors that cause abnormal brain–gut interaction in diarrhea-predominant irritable bowel syndrome (IBS-D). Recently, it was found that the imbalance of the gut microbiota–bile acid axis is closely related to them. Therefore, understanding the structure and function of the gut microbiota and bile acids and the underlying mechanisms by which they shape visceral hypersensitivity and mucosal barrier damage in IBS-D is critical. An examination of intestinal feces from IBS-D patients revealed that alterations in gut microbiota and bile acid metabolism underlie IBS-D and symptom onset. We also expanded beyond existing knowledge of well-studied gut microbiota and bile acid and found that Bacteroides ovatus and chenodeoxycholic acid may be potential bacteria and bile acid involved in the pathogenesis of IBS-D. Moreover, our data integration reveals the influence of the microbiota–bile acid–TGR5 axis on barrier function and visceral hypersensitivity.
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