Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Deutsches Zentrum für Immuntherapie, Friedrich-Alexander-University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany.
Nat Rev Rheumatol. 2021 Apr;17(4):224-237. doi: 10.1038/s41584-021-00585-3. Epub 2021 Mar 5.
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disorder that primarily affects the joints. One hypothesis for the pathogenesis of RA is that disease begins at mucosal sites as a consequence of interactions between the mucosal immune system and an aberrant local microbiota, and then transitions to involve the synovial joints. Alterations in the composition of the microbial flora in the lungs, mouth and gut in individuals with preclinical and established RA suggest a role for mucosal dysbiosis in the development and perpetuation of RA, although establishing whether these alterations are the specific consequence of intestinal involvement in the setting of a systemic inflammatory process, or whether they represent a specific localization of disease, is an ongoing challenge. Data from mouse models of RA and investigations into the preclinical stages of disease also support the hypothesis that these alterations to the microbiota predate the onset of disease. In addition, several therapeutic options widely used for the treatment of RA are associated with alterations in intestinal microbiota, suggesting that modulation of intestinal microbiota and/or intestinal barrier function might be useful in preventing or treating RA.
类风湿关节炎（RA）是一种慢性自身免疫性炎症性疾病，主要影响关节。RA 发病机制的一个假说认为，疾病首先在黏膜部位发生，是黏膜免疫系统和异常局部微生物群之间相互作用的结果，然后转移到滑膜关节。临床前和确诊的 RA 患者的肺部、口腔和肠道微生物菌群组成发生改变，提示黏膜微生态失调在 RA 的发生和持续中起作用，尽管确定这些改变是肠道受累在全身性炎症过程中的特定后果，还是代表疾病的特定定位，仍然是一个持续的挑战。来自 RA 小鼠模型的数据以及对疾病临床前阶段的研究也支持这样一种假说，即这些微生物群的改变先于疾病的发生。此外，几种广泛用于治疗 RA 的治疗选择与肠道微生物群的改变有关，这表明调节肠道微生物群和/或肠道屏障功能可能有助于预防或治疗 RA。
