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不仅仅是一个泄漏的肠道:肠道化如何塑造关节炎

Kristine A Kuhn¹, Kentaro Yomogida², Kathryn Knoop³

¹Division of Rheumatology, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. kristine.kuhn@cuanschutz.edu.

Nature reviews. Rheumatology

|July 31, 2025

概括

肠道微生物组的变化 (失生症) 可能引发免疫功能障碍,导致类风湿性关节炎和脊椎关节炎. 研究探讨了诸如分子模仿和微生物转位等机制,这些机制与微生物转位不同.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
胃肠病学胃肠病学

背景情况:

肠道微生物群对宿主健康至关重要,影响消化,免疫和病原体保护.
肠道微生物组的变化与类风湿性关节炎 (RA) 和脊柱性关节炎 (SpA) 等炎症状况有关.
肠关节假设提出,肠道失调驱动免疫功能障碍,导致关节炎的发展.

研究的目的:

探索肠道失生症可能引发关节炎的机制.
批判性地评估支持拟议机制的证据.
为了澄清误解和识别肠-关节轴研究中的知识差距.

主要方法:

关于RA和SPA肠道微生物组变化的现有科学文献的审查和综合.
分析包括分子模仿,粘膜免疫失调,微生物转移,代谢物生产和免疫细胞贩运在内的拟议机制.
对支持每个机制的数据进行批判性评估,突出限制和未来研究领域.

主要成果:

几种机制将肠道失调与关节炎联系起来,包括分子模仿和微生物转移.
术语"漏肠"是不鼓励的;肠道透性和细菌转移具有明显的免疫效应.
关节炎的发展可能涉及多种途径的融合,可能在个体和疾病亚型之间有所不同.

结论:

肠道失生症通过各种不同的机制与RA和SPA的发病有关.
需要使用模型生物和干预试验进行进一步的研究,以单独和集体验证这些机制.
澄清这些途径对于进一步了解和开发炎症性关节炎的向疗法至关重要.

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