Department of Rheumatology and Immunology, Rare Diseases Center, Institute of Immunology and Inflammation, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, China.
Department of Laboratory Medicine and Outpatient, West China Hospital, Sichuan University, Chengdu, China.
Front Immunol. 2021 Jul 15;12:686501. doi: 10.3389/fimmu.2021.686501. eCollection 2021.
Systemic lupus erythematosus (SLE), often considered the prototype of autoimmune diseases, is characterized by over-activation of the autoimmune system with abnormal functions of innate and adaptive immune cells and the production of a large number of autoantibodies against nuclear components. Given the highly complex and heterogeneous nature of SLE, the pathogenesis of this disease remains incompletely understood and is presumed to involve both genetic and environmental factors. Currently, disturbance of the gut microbiota has emerged as a novel player involved in the pathogenesis of SLE. With in-depth research, the understanding of the intestinal bacteria-host interaction in SLE is much more comprehensive. Recent years have also seen an increase in metabolomics studies in SLE with the attempt to identify potential biomarkers for diagnosis or disease activity monitoring. An intricate relationship between gut microbiome changes and metabolic alterations could help explain the mechanisms by which gut bacteria play roles in the pathogenesis of SLE. Here, we review the role of microbiota dysbiosis in the aetiology of SLE and how intestinal microbiota interact with the host metabolism axis. A proposed treatment strategy for SLE based on gut microbiome (GM) regulation is also discussed in this review. Increasing our understanding of gut microbiota and their function in lupus will provide us with novel opportunities to develop effective and precise diagnostic strategies and to explore potential microbiota-based treatments for patients with lupus.
系统性红斑狼疮(SLE)通常被认为是自身免疫性疾病的典型代表,其特征是自身免疫系统过度激活,先天和适应性免疫细胞功能异常,以及产生大量针对核成分的自身抗体。鉴于 SLE 的高度复杂和异质性,其发病机制仍不完全清楚,据推测与遗传和环境因素有关。目前,肠道微生物群的紊乱已成为参与 SLE 发病机制的新因素。随着深入研究,对 SLE 中肠道细菌-宿主相互作用的理解更加全面。近年来,SLE 中的代谢组学研究也有所增加,试图确定用于诊断或疾病活动监测的潜在生物标志物。肠道菌群变化和代谢改变之间错综复杂的关系可以帮助解释肠道细菌在 SLE 发病机制中发挥作用的机制。在这里,我们回顾了肠道菌群失调在 SLE 发病机制中的作用,以及肠道微生物群如何与宿主代谢轴相互作用。本文还讨论了基于肠道微生物群(GM)调节的 SLE 治疗策略。增加我们对肠道微生物群及其在狼疮中的功能的理解将为我们提供新的机会,以开发有效的、精准的诊断策略,并探索基于微生物群的狼疮患者的潜在治疗方法。
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