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Abstract：
The present study aimed to explore the underlying mechanism of bile reflux-inducing chronic atrophic gastritis (CAG) with colonic mucosal lesion. The rat model of CAG with colonic mucosal lesion was induced by free-drinking 20 mmol/L sodium deoxycholate to simulate bile reflux and 2% cold sodium salicylate for 12 weeks. In comparison to the control group, the model rats had increased abundances of Bacteroidetes and Firmicutes but had decreased abundances of Proteobacteria and Fusobacterium. Several gut bacteria with bile acids transformation ability were enriched in the model group, such as Blautia, Phascolarctobacter, and Enterococcus. The cytotoxic deoxycholic acid and lithocholic acid were significantly increased in the model group. Transcriptome analysis of colonic tissues presented that the down-regulated genes enriched in T cell receptor signaling pathway, antigen processing and presentation, Th17 cell differentiation, Th1 and Th2 cell differentiation, and intestinal immune network for IgA production in the model group. These results suggest that bile reflux-inducing CAG with colonic mucosal lesion accompanied by gut dysbacteriosis, mucosal immunocompromise, and increased gene expressions related to repair of intestinal mucosal injury.
摘要：
本研究旨在探讨胆汁反流诱发慢性萎缩性胃炎(CAG)结肠黏膜病变的机制。用自由饮用20mmol/L脱氧胆酸钠模拟胆汁反流和2％冷水杨酸钠，连续12周建立大鼠结肠粘膜损伤的CAG模型。与对照组相比，模型大鼠的拟杆菌和厚壁菌的丰度增加，但变形杆菌和梭杆菌的丰度降低。模型组富集了几种具有胆汁酸转化能力的肠道细菌,比如Blautia,相枯病杆菌,和肠球菌.模型组细胞毒性脱氧胆酸和石胆酸明显升高。结肠组织的转录组分析显示，下调的基因富含T细胞受体信号通路，抗原加工和呈递，Th17细胞分化，Th1和Th2细胞分化，模型组IgA生产的肠道免疫网络。这些结果表明，胆汁反流诱导的CAG伴有结肠粘膜病变并伴有肠道菌群失调，粘膜免疫妥协，肠粘膜损伤修复相关基因表达增加。
