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由Odoribacter Splanchnicus修饰的二次胆汁酸通过抑制中性细胞外细胞陷形成来缓解结肠炎

Jing Xu^1,2, Jianhong Li^1,2, Xue Guo^1,2

¹Department of Gastroenterology and Hepatology, the Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|September 24, 2025

概括

在炎症性肠病 (IBD) 中消耗的Odoribacter splanchnicus,可以保护小鼠免受大肠炎的侵害. 它通过增加石英酸 (LCA) 来降低炎症,这抑制了中性粒细胞外细胞陷 (NET) 的形成.

科学领域:

微生物学微生物学
免疫学免疫学免疫学
胃肠病学胃肠病学

背景情况:

肠道微生物群在炎症性肠病 (IBD) 中的作用很重要,但细菌物种的特定功能尚未完全理解.
识别关键的细菌种群及其在IBD病原体中的机制对于开发向疗法至关重要.

研究的目的:

在炎症性肠病 (IBD) 模型中研究Odoribacter splanchnicus (O. splanchnicus) 的保护作用.
阐明O. splanchnicus发挥抗炎作用的机制,重点关注中性粒细胞外细胞陷 (NET) 和胆酸代谢.

主要方法:

在急性和慢性小鼠结肠炎模型中使用O. splanchnicus.
评估结肠炎症,屏障完整性,粘膜免疫格局和NETs形成.
代谢分析,以识别关键代谢物,包括胆酸.
补充研究使用石灰酸 (LCA) 和便微生物群移植 (FMT).
对NLRP3-GSDMD信号通路的研究.

主要成果:

在小鼠中,O. splanchnicus的使用显著缓解了结肠炎症,并改善了屏障完整性.
O. splanchnicus的治疗减少了NETs的形成,这取决于宿主的NETs机制 (Pad4).
治疗以微生物群依赖的方式增加了二次胆汁酸石化酸 (LCA) 的水平.
通过抑制NLRP3-GSDMD通路,LCA补充效应模仿了anti-NETs效应并抑制了炎症.

结论:

臭菌splanchnicus具有对大肠炎的保护作用,通过微生物群依赖的LCA的产生进行介导.
通过NLRP3-GSDMD通路抑制NETs形成,LCA可以抑制结肠炎症.
这些发现确定了肠道微生物群-代谢物-中性粒细胞轴在IBD病变发生过程中至关重要,并强调LCA是关键的保护因素.

关键词:

我们的肠道微生物群.中性粒细胞外细胞陷臭虫菌是splanchnicuscus的意思,因为它具有臭味.二次胆汁酸二次胆汁酸性结肠炎是一种

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