肠道微生物群通过激活NAD+救援途径来影响抗TNF反应性 性结肠炎
1Department of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|December 31, 2024
概括
肠道细菌影响性结肠炎的治疗反应. Fusobacterium nucleatum通过影响NAD+代谢来增加炎症,可能导致对抗瘤坏死因子 (TNF) 疗法的耐药性.
科学领域:
- 胃肠病学 胃肠病学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 性结肠炎 (UC) 治疗对抗瘤缩因子 (TNF) 治疗的耐药性影响大约50%的患者.
- 肠道微生物群在UC抗TNF治疗耐药性的作用是显著的,但在机制上不清楚.
研究的目的:
- 为了研究肠道微生物群对性结肠炎中抗TNF治疗反应的影响.
- 阐明肠道细菌对UC中抗TNF治疗耐药性的机制.
主要方法:
- 从UC患者的便微生物群移植到硫酸诱导的大肠炎小鼠模型中.
- 在UC患者和小鼠中分析肠道微生物群组成和代谢物概况.
- 研究Fusobacterium nucleatum感染对NCM460细胞和炎症通路的影响.
主要成果:
- 来自UC的微生物群移植改变了小鼠的肠道微生物群多样性和因弗力西马布的响应性.
- 在非响应性UC患者中观察到Romboutsia和Fusobacterium的丰度增加.
- 菌核酸菌感染上调了NAMPT,激活了p38 MAPK通路,并通过NAD+代谢促进炎症.
结论:
- 肠道微生物群的组成显著影响抗TNF治疗在性结肠炎的疗效.
- 菌核酸通过NAD+救援通路激活促进炎症和抗TNF药物耐药性.
- 针对F. nucleatum和相关的代谢途径提供了潜在的治疗策略,以克服UC治疗耐药性.
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