肺肠轴微生物如何调节COPD免疫?2024机制详解与临床意义

昨天 MedSci xAi 发表于广东省
本文深度解析肺肠轴微生物群在COPD免疫调节中的关键作用,涵盖分段丝状细菌SFB的免疫激活机制、益生菌的屏障保护功能,以及SCFAs和LPS等代谢物通过TLR4通路诱导炎症的具体分子机制,为临床干预提供新靶点。
The respiratory and gastrointestinal mucosal microbiota serve as the biological foundation for the bidirectional interaction of the “lung-gut” axis. The gut microbiota can influence the development and progression of COPD by modulating immune function. Specific bacterial populations, such as segmented filamentous bacteria (SFB), can directly adhere to intestinal epithelial cells, activating both innate and adaptive immune cells, inducing immune cell differentiation, promoting lymphoid tissue development, and IgA production, thereby maintaining host barrier protection and self-immune balance [53]. Probiotics such as bifidobacteria and lactobacilli can inhibit the colonization of harmful bacteria through the formation of a biological barrier, production of antimicrobial substances, enhancement of antibody levels, and activation of macrophages. The gut mucosal immune system is interconnected with the respiratory mucosal immune system via the common mucosal immune system. When immune function is weakened, opportunistic pathogens can more easily infect and cause pulmonary inflammation or exacerbate existing conditions [47]. Additionally, microbial metabolites (such as short-chain fatty acids, SCFAs, and lipopolysaccharides, LPS) are key mediators in the crosstalk between the lung and gut. LPS, in particular, can enter the bloodstream following gut barrier damage and induce inflammatory responses by activating TLR4 receptors on immune cells [54,55].
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