失调
肠道菌群
胆汁酸
炎症性肠病
厚壁菌
发病机制
胃肠道
生物
微生物学
内科学
脱氧胆酸
免疫学
疾病
医学
细菌
生物化学
遗传学
16S核糖体RNA
作者
Min Yang,Yu Gu,Lingfeng Li,Tianyu Li,Xueli Song,Yue Sun,Xiaocang Cao,Bangmao Wang,Kui Jiang,Hailong Cao
出处
期刊:Nutrients
[MDPI AG]
日期:2021-09-09
卷期号:13 (9): 3143-3143
被引量:72
摘要
Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disorder of the gastrointestinal tract, with increasing prevalence, and its pathogenesis remains unclear. Accumulating evidence suggested that gut microbiota and bile acids play pivotal roles in intestinal homeostasis and inflammation. Patients with IBD exhibit decreased microbial diversity and abnormal microbial composition marked by the depletion of phylum Firmicutes (including bacteria involved in bile acid metabolism) and the enrichment of phylum Proteobacteria. Dysbiosis leads to blocked bile acid transformation. Thus, the concentration of primary and conjugated bile acids is elevated at the expense of secondary bile acids in IBD. In turn, bile acids could modulate the microbial community. Gut dysbiosis and disturbed bile acids impair the gut barrier and immunity. Several therapies, such as diets, probiotics, prebiotics, engineered bacteria, fecal microbiota transplantation and ursodeoxycholic acid, may alleviate IBD by restoring gut microbiota and bile acids. Thus, the bile acid–gut microbiota axis is closely connected with IBD pathogenesis. Regulation of this axis may be a novel option for treating IBD.
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