详细信息
Mechanistic insights into how gut homeostasis and immune-system crosstalk shape ankylosing spondylitis ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Mechanistic insights into how gut homeostasis and immune-system crosstalk shape ankylosing spondylitis
作者:Li, Jiawen[1];Xie, Xingwen[1]
第一作者:李佳蔚
通信作者:Xie, XW[1]
机构:[1]Gansu Univ Tradit Chinese Med, Lanzhou, Peoples R China
第一机构:甘肃中医药大学
通信机构:[1]corresponding author), Gansu Univ Tradit Chinese Med, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;
年份:2026
卷号:17
外文期刊名:FRONTIERS IN IMMUNOLOGY
收录:;WOS:【SCI-EXPANDED(收录号:WOS:001798664600001)】;
基金:The author(s) declared that financial support was received for this work and/or its publication. This research was supported by the Gansu University of Chinese Medicine Graduate Innovation and Entrepreneurship Fund (No. 2025CXCY-015, No. 2025CXZX-927, No. 2025CXZX-914), the Lanzhou Talent Innovation and Entrepreneurship Project (No. 2024-RC-89), and the Open Fund of the State Key Laboratory of Chinese Medicine Performance Innovation Engineering (No. SKL2025-11).Gansu University of Chinese Medicine Research Project, Key Scientific Research Project: GZKZ-2024-9; National Natural Science Foundation Project: No. 82374491; National Natural Science Foundation Projects: No. 82160918, 82160911; Gansu Provincial Science and Technology Plan Key R&D Project (No. 26YFFA031).
语种:英文
外文关键词:ankylosing spondylitis; gut;joint axis; gut microbiota; intestinal barrier dysfunction; microbial metabolites; mucosal immunity
摘要:Ankylosing spondylitis (AS) is a chronic immune-mediated inflammatory disease that primarily affects the axial skeleton and entheseal structures. Although the role of HLA-B27 is well established, AS pathogenesis is multifactorial, and accumulating evidence suggests that disruption of intestinal homeostasis and the gut-joint axis may contribute to disease pathobiology. AS-associated gut dysbiosis is characterized by reduced microbial diversity and compositional alterations that may be associated with mucosal immune activation, increased intestinal permeability, and systemic inflammatory priming. Mechanistically, altered microbial signals and barrier dysfunction may converge on key immunological pathways, including the IL-23/IL-17 axis, and may promote the activation or trafficking of innate-like lymphocytes, such as MAIT cells, gamma delta T cells, and ILC3s, thereby contributing to inflammation and abnormal bone remodeling. In addition to community structure, microbial metabolites, including short-chain fatty acids and tryptophan-derived indole metabolites, help regulate epithelial integrity and immunoregulatory homeostasis; their perturbation may favor pro-inflammatory immune programs relevant to AS. This review summarizes recent evidence on dysbiosis, barrier dysfunction, and immunometabolic signaling in the gut-joint axis, while critically distinguishing established immune-targeted therapies from experimental microbiota-directed and combination strategies.
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