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肠道微生物组在膝骨关节炎中的免疫作用:可能机制和治疗方法的综述。

The immune role of the intestinal microbiome in knee osteoarthritis: a review of the possible mechanisms and therapies.

机构信息

Department of Orthopedics, Nanjing Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

出版信息

Front Immunol. 2023 Jun 14;14:1168818. doi: 10.3389/fimmu.2023.1168818. eCollection 2023.

DOI:10.3389/fimmu.2023.1168818
PMID:37388748
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10306395/
Abstract

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by cartilage damage and synovial inflammation and carries an enormous public health and economic burden. It is crucial to uncover the potential mechanisms of OA pathogenesis to develop new targets for OA treatment. In recent years, the pathogenic role of the gut microbiota in OA has been well recognized. Gut microbiota dysbiosis can break host-gut microbe equilibrium, trigger host immune responses and activate the "gut-joint axis", which aggravates OA. However, although the role of the gut microbiota in OA is well known, the mechanisms modulating the interactions between the gut microbiota and host immunity remain unclear. This review summarizes research on the gut microbiota and the involved immune cells in OA and interprets the potential mechanisms for the interactions between the gut microbiota and host immune responses from four aspects: gut barrier, innate immunity, adaptive immunity and gut microbiota modulation. Future research should focus on the specific pathogen or the specific changes in the gut microbiota composition to identify the related signaling pathways involved in the pathogenesis of OA. In addition, future studies should include more novel interventions on immune cell modifications and gene regulation of specific gut microbiota related to OA to validate the application of gut microbiota modulation in the onset of OA.

摘要

骨关节炎(OA)是一种慢性退行性关节疾病,其特征为软骨损伤和滑膜炎症,给公共健康和经济带来了巨大负担。揭示 OA 发病机制的潜在机制对于开发 OA 治疗的新靶点至关重要。近年来,肠道微生物群在 OA 中的致病作用已得到充分认识。肠道微生物群失调会打破宿主-肠道微生物平衡,引发宿主免疫反应并激活“肠道-关节轴”,从而加重 OA。然而,尽管肠道微生物群在 OA 中的作用已广为人知,但调节肠道微生物群与宿主免疫相互作用的机制仍不清楚。本综述总结了肠道微生物群与 OA 相关免疫细胞的研究,并从肠道屏障、先天免疫、适应性免疫和肠道微生物群调节四个方面解释了肠道微生物群与宿主免疫反应相互作用的潜在机制。未来的研究应集中于特定病原体或肠道微生物群组成的特定变化,以确定与 OA 发病机制相关的特定信号通路。此外,未来的研究应包括更多关于免疫细胞修饰和与 OA 相关的特定肠道微生物群基因调节的新干预措施,以验证肠道微生物群调节在 OA 发病中的应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/d01a621c7df7/fimmu-14-1168818-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/b369017b3ab4/fimmu-14-1168818-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/06ef997f163c/fimmu-14-1168818-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/a5f705fc4da9/fimmu-14-1168818-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/d01a621c7df7/fimmu-14-1168818-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/b369017b3ab4/fimmu-14-1168818-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/06ef997f163c/fimmu-14-1168818-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/a5f705fc4da9/fimmu-14-1168818-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fcc5/10306395/d01a621c7df7/fimmu-14-1168818-g004.jpg

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