Succinate and inosine coordinate innate immune response to bacterial infection

文献类型： 外文期刊

第一作者： Jiang, Ming

作者： Jiang, Ming;Chen, Zhuang-gui;Li, Hui;Zhang, Tian-tuo;Yang, Man-jun;Peng, Xuan-xian;Peng, Bo;Jiang, Ming;Peng, Bo;Jiang, Ming

作者机构：

期刊名称：PLOS PATHOGENS （ 影响因子：6.7； 五年影响因子：6.7 ）

ISSN： 1553-7366

年卷期： 2022 年 18 卷 8 期

页码：

收录情况： SCI

摘要： Macrophages restrict bacterial infection partly by stimulating phagocytosis and partly by stimulating release of cytokines and complement components. Here, we treat macrophages with LPS and a bacterial pathogen, and demonstrate that expression of cytokine IL-1 beta and bacterial phagocytosis increase to a transient peak 8 to 12 h post-treatment, while expression of complement component 3 (C3) continues to rise for 24 h post-treatment. Metabolomic analysis suggests a correlation between the cellular concentrations of succinate and IL-1 beta and of inosine and C3. This may involve a regulatory feedback mechanism, whereby succinate stimulates and inosine inhibits HIF-1 alpha through their competitive interactions with prolyl hydroxylase. Furthermore, increased level of inosine in LPS-stimulated macrophages is linked to accumulation of adenosine monophosphate and that exogenous inosine improves the survival of bacterial pathogen-infected mice and tilapia. The implications of these data suggests potential therapeutic tools to prevent, manage or treat bacterial infections.

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