Staphylococcus aureus Conquers Host by Hijacking Mitochondria via PFKFB3 in Epithelial Cells

文献类型： 外文期刊

第一作者： Gao, Xing

作者： Gao, Xing;Wu, Binfeng;Liu, Laizhen;Xu, Yuanyuan;Miao, Jinfeng;Feng, Shiyuan;Zhang, Jinqiu;Zhang, Jinqiu

作者机构：

关键词： glycolysis; SIRT3-HIF1 alpha; mitophagy; PFKFB3; Staphylococcus aureus

期刊名称：JOURNAL OF INFECTIOUS DISEASES （ 影响因子：6.4； 五年影响因子：5.4 ）

ISSN： 0022-1899

年卷期： 2024 年

页码：

收录情况： SCI

摘要： Staphylococcus aureus persists within mammary epithelial cells for an extended duration, exploiting the host metabolic resources to facilitate replication. This study revealed a mechanism by which intracellular S aureus reprograms host metabolism, with PFKFB3 playing a crucial role in this process. Mechanistically, S aureus induced mitochondrial damage, leading to increased levels of mitochondrial reactive oxygen species and dysfunction in the electron transport chain. Moreover, S aureus shifted the balance of mitochondrial dynamics from fusion to fission, subsequently activating PINK1-PRKN-dependent mitophagy, causing loss of sirtuin 3 to stabilize hypoxic inducible factor 1 alpha, and shifting the host metabolism toward enhanced glycolysis. The inhibition of PFKFB3 reversed the mitochondrial damage and degradation of sirtuin 3 induced by S aureus. Overall, our findings elucidate the mechanism by which S aureus reprograms host metabolism, thereby offering insights into the treatment of S aureus infection. Staphylococcus aureus induced sirtuin 3 degradation via mitophagy, thereby shifting metabolism toward glycolysis. Inhibition of PFKFB3 reduced mitochondrial damage by limiting reactive oxygen species production and alleviated the degradation of sirtuin 3.

分类号：

  • 相关文献
作者其他论文 更多>>

微信小程序