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脊柱关节炎中的肠道

The gut in spondyloarthritis.

作者信息

Wendling Daniel

机构信息

Service de Rhumatologie, CHRU de Besançon, et Université de Franche-Comté, boulevard Fleming, 25030 Besançon, France.

出版信息

Joint Bone Spine. 2016 Jul;83(4):401-5. doi: 10.1016/j.jbspin.2016.02.017. Epub 2016 Apr 14.

Abstract

The links between the bowel and spondyloarthritis, although demonstrated many years ago, have been placed under the spotlight by recent findings. Thus, studies have established that bowel inflammation is associated with the joint disease activity, sacroiliac joint inflammation by magnetic resonance imaging, and elevated levels of biomarkers for bowel inflammation (S100 proteins) or antimicrobial antibodies (anti-flagellin). IL-23/Th17 pathway activation originating in the bowel has been documented in studies demonstrating that lymphoid cells expressing the IL-23 receptor can migrate to the bloodstream, bone marrow, and joints, via a mechanism involving adhesion molecules. Bacteria present in the bowel are increasingly emerging as major players. Thus, dysbiosis of the bowel microbiota can induce IL-23 production and local inflammatory responses. These new data suggest avenues of research for future treatments.

摘要

肠道与脊柱关节炎之间的联系,尽管在多年前就已得到证实,但最近的研究结果使其备受关注。因此,研究已经证实肠道炎症与关节疾病活动、磁共振成像显示的骶髂关节炎症以及肠道炎症生物标志物(S100蛋白)或抗微生物抗体(抗鞭毛蛋白)水平升高有关。在一些研究中已经记录到起源于肠道的IL-23/Th17通路激活,这些研究表明表达IL-23受体的淋巴细胞可通过一种涉及黏附分子的机制迁移至血液、骨髓和关节。肠道中存在的细菌越来越多地成为主要因素。因此,肠道微生物群失调可诱导IL-23产生和局部炎症反应。这些新数据为未来的治疗研究提供了方向。

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