The First Affiliated Hospital of Harbin Medical University, Harbin, China.
The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Microb Pathog. 2022 Dec;173(Pt A):105803. doi: 10.1016/j.micpath.2022.105803. Epub 2022 Oct 15.
Ulcerative colitis (UC) is a chronic inflammatory disease of the intestine. It is characterized with recurrent. The pathogenesis is mainly associated with environmental factors, genetic susceptibility, dysbiosis of the intestinal flora and autoimmunity. The role of intestinal flora disorders in the pathogenesis and progression of UC is becoming increasingly prominent. More and more studies have confirmed that fecal microbiota transplantation (FMT) could reshape the composition of UC intestinal flora and it is expected to be a new strategy for UC treatment. In this study, we used 2% Dextran sulfate sodium (DSS) for 7 days to induce acute colitis model in mice, and interfere with FMT and Enterotoxigenic Escherichia coli (ETEC). ELISA and immunohistochemistry were applied to detect the concentration and expression of NF-κB p65, STAT3 and IL-6. 16SrRNA high-throughput sequencing was performed to explore the composition of intestinal flora. The aim was to study the treatment effect of FMT on UC mice and explore its potential mechanism by observing the changes of intestinal flora composition and diversity, and its relationship with NF-κB p65, STAT3 and IL-6 expression. We conclude that FMT could improve intestinal flora disorder in mice with ulcerative colitis, regulate NF-κB signaling pathway, and significantly reduce intestinal inflammation in UC mice.
溃疡性结肠炎(UC)是一种慢性肠道炎症性疾病。它具有反复发作的特点。其发病机制主要与环境因素、遗传易感性、肠道菌群失调和自身免疫有关。肠道菌群失调在 UC 的发病机制和进展中的作用日益突出。越来越多的研究证实,粪便微生物移植(FMT)可以重塑 UC 肠道菌群的组成,有望成为 UC 治疗的新策略。在本研究中,我们使用 2%葡聚糖硫酸钠(DSS)诱导小鼠急性结肠炎模型 7 天,并进行 FMT 和肠产毒性大肠杆菌(ETEC)干预。采用 ELISA 和免疫组织化学方法检测 NF-κB p65、STAT3 和 IL-6 的浓度和表达。采用 16SrRNA 高通量测序技术探索肠道菌群的组成。目的是通过观察肠道菌群组成和多样性的变化及其与 NF-κB p65、STAT3 和 IL-6 表达的关系,研究 FMT 对 UC 小鼠的治疗效果及其潜在机制。我们得出结论,FMT 可以改善溃疡性结肠炎小鼠的肠道菌群紊乱,调节 NF-κB 信号通路,显著减轻 UC 小鼠的肠道炎症。