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Serine protease Rv2569c inhibits inflammatory response and promotes intracellular survival of Mycobacterium tuberculosis by targeting the RhoG-NF-κB-NLRP3 pathway

文献类型： 外文期刊

作者： Xinxin Zang;Jiajun Zhang;Tingting Feng;Hui Wang;Yingying Cui;Yanyan Jiang;Chunwen Chen;Siguo Liu;Guanghui Dang

作者机构：

关键词： Mycobacterium tuberculosis Rv2569c;NF-κB signaling pathway;NLRP3 inflammasome

期刊名称： International Journal of Biological Macromolecules

ISSN： 0141-8130

年卷期： 2025 年 309 卷

页码：

收录情况： SCIE（2025版） ; ; EI（2025版）

摘要： Innate immunity is dominant in protecting the host's defense against intracellular bacterial infections. The secretion of IL-1β and activation of NLRP3 inflammasome in macrophages play a critical role in combating Mycobacterium tuberculosis (M.tb) infections. M.tb is an extremely successful intracellular pathogen that evades host innate immunity by interfering with a wide range of macrophage functions. However, the precise infection mechanism remains unclear. This study demonstrates that the mycobacterial serine protease Rv2569c interacts with RhoG in macrophages, effectively blocking the NF-κB signaling pathway's initiation and suppressing NLRP3 inflammasome activation, ultimately leading to a decrease in IL-1β secretion and promoting mycobacterial survival within macrophages. To investigate the role of Rv2569c in M.tb infection, an Rv2569c-deficient strain (H37RvΔRv2569c) was used to demonstrate a weakened suppression of the inflammatory response and lower intracellular survival compared to the wild-type (H37Rv) and complemented strain (H37RvΔRv2569c + Rv2569c) through in vitro and in vivo experiments. The findings provide the first proof that RhoG serves as an endogenous host sensor for pathogens and that Rv2569c-RhoG-mediated inflammatory response plays a crucial role in mycobacterial immune evasion.

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