沙门氏菌感染过程中 B 细胞的促炎和抗炎反应

European journal of microbiology & immunology Pub Date : 2025-03-11 Print Date: 2025-03-19 DOI:10.1556/1886.2024.00088
Araceli Perez-Lopez, Gabriela Hernandez-Galicia, Luis Uriel Lopez-Bailon, Ana D Gonzalez-Telona, Roberto Rosales-Reyes, Celia M Alpuche-Aranda, Jose I Santos-Preciado, Vianney Ortiz-Navarrete
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引用次数: 0

摘要

b细胞作为沙门氏菌建立慢性感染的生态位,使细菌能够逃避免疫反应。沙门氏菌在b细胞内存活的一种机制包括抑制NLRC4炎性体的激活,从而防止热腐细胞死亡。本研究探讨沙门氏菌感染的b细胞是否能产生杀菌反应来控制细胞内细菌。我们的研究结果表明,沙门氏菌感染的b细胞可以产生和释放TNFα、IL-6和IL-10,但不产生RANTES。此外,用TNFα、IL-1β或IFNγ注入b细胞,通过促进活性氧和产氮物种的产生,减少细胞内负荷,增强了它们的杀菌活性。这些结果表明b细胞可以在促炎环境中清除沙门氏菌感染。然而,同时产生的IL-10可能会抵消促炎细胞因子的作用,潜在地调节微环境中的免疫反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pro-inflammatory and anti-inflammatory responses in B cells during Salmonella infection.

B-cells serve as a niche for Salmonella to establish a chronic infection, enabling bacteria to evade immune responses. One mechanism Salmonella uses to survive inside B-cells involves inhibiting the NLRC4 inflammasome activation, thereby preventing pyroptotic cell death. This study investigates whether Salmonella-infected B-cells can mount bactericidal responses to control intracellular bacteria. Our results show that Salmonella-infected B-cells can produce and release TNFα, IL-6, and IL-10, but not RANTES. Furthermore, priming B-cells with TNFα, IL-1β, or IFNγ enhances their bactericidal activity by promoting the production of reactive oxygen and nitrogen production species, reducing intracellular load. These results suggest that B-cells can clear Salmonella infection within a pro-inflammatory environment. However, the concurrent production of IL-10 may counteract the effects of pro-inflammatory cytokines, potentially modulating the immune response in the microenvironment.

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