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Succinate and inosine coordinate innate immune response to bacterial infection

文献类型： 外文期刊

作者： Jiang, Ming 1 ; Chen, Zhuang-gui 1 ; Li, Hui 1 ; Zhang, Tian-tuo 1 ; Yang, Man-jun 1 ; Peng, Xuan-xian 1 ; Peng, Bo 1 ;

作者机构： 1.Sun Yat Sen Univ, Higher Educ Mega Ctr,State Key Lab Biocontrol, Southern Marine Sci & Engn Guangdong Lab Zhuhai,C, Sch Life Sci,Guangdong Key Lab Pharmaceut Funct G, Guangzhou, Peoples R China

2.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China

3.Guangdong Acad Agr Sci, Inst Anim Sci, Guangzhou, Peoples R China

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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