Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, 712100, China.
College of Veterinary Medicine, Northwest A&F University, Yangling, 712100, China.
NPJ Biofilms Microbiomes. 2023 Aug 14;9(1):56. doi: 10.1038/s41522-023-00420-5.
Inflammatory bowel disease (IBD) is associated with gut dysbiosis and can lead to colitis-associated malignancies. Bacteroides uniformis (Bu) regulates animal intestinal homeostasis; however, the mechanism by which it alleviates colitis in mice remains unknown. We investigated the effects of B. uniformis JCM5828 and its metabolites on female C57BL/6J mice with dextran sulfate sodium salt (DSS) induced colitis. Treatment with Bu considerably alleviated colitis progression and restored the mechanical and immune barrier protein expression. Additionally, Bu increased the abundance of the symbiotic bacteria Bifidobacterium and Lactobacillus vaginalis while decreasing that of pathogenic Escherichia-Shigella, and modulated intestinal bile acid metabolism. Bu largely regulated the expression of key regulatory proteins of the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways in colonic tissues and the differentiation of TH17 cells. However, Bu could not directly inhibit TH17 cell differentiation in vitro; it modulated the process in the lamina propria by participating in bile acid metabolism and regulating key metabolites (alpha-muricholic, hyodeoxycholic, and isolithocholic acid), thereby modulating the intestinal immune response. Our findings suggest that Bu or bile acid supplements are potential therapies for colitis and other diseases associated with intestinal barrier dysfunction.
炎症性肠病（IBD）与肠道菌群失调有关，并可导致结肠炎相关的恶性肿瘤。均匀拟杆菌（Bu）调节动物肠道内稳态；然而，其缓解小鼠结肠炎的机制尚不清楚。我们研究了均匀拟杆菌 JCM5828 及其代谢产物对葡聚糖硫酸钠（DSS）诱导的结肠炎雌性 C57BL/6J 小鼠的影响。Bu 的治疗显著缓解了结肠炎的进展，并恢复了机械和免疫屏障蛋白的表达。此外，Bu 增加了共生细菌双歧杆菌和阴道乳杆菌的丰度，同时减少了致病性大肠杆菌-志贺氏菌的丰度，并调节了肠道胆汁酸代谢。Bu 大量调节了结肠组织中 NF-κB 和丝裂原活化蛋白激酶（MAPK）信号通路的关键调节蛋白的表达以及 TH17 细胞的分化。然而，Bu 不能直接抑制体外 TH17 细胞的分化；它通过参与胆汁酸代谢和调节关键代谢物（alpha-鼠胆酸、去氧胆酸和异石胆酸）来调节固有层中的这一过程，从而调节肠道免疫反应。我们的研究结果表明，Bu 或胆汁酸补充剂可能是治疗结肠炎和其他与肠道屏障功能障碍相关疾病的潜在疗法。
