STING contributes to the inflammation and proliferation of Staphylococcus aureus via mitochondrial reactive oxygen species-hypoxic inducible factor 1α axis in epithelial cells

文献类型： 外文期刊

第一作者： Gao, Xing

作者： Gao, Xing;Wu, Binfeng;Qiu, Yawei;Miao, Jinfeng;Feng, Shiyuan;Zhang, Jinqiu;Zhang, Jinqiu

作者机构：

关键词： STING; mastitis; mROS-HIF1 alpha; glycolysis; Staphylococcus aureus

期刊名称：INFECTION AND IMMUNITY （ 影响因子：2.8； 五年影响因子：3.1 ）

ISSN： 0019-9567

年卷期： 2025 年 93 卷 6 期

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收录情况： SCI

摘要： Staphylococcus aureus infection poses a serious threat to the dairy industry and public health safety. The stimulator of interferon gene (STING) signaling pathway has been well established as effective in defending against viral infections. However, the role of STING is controversial during bacterial infections. Herein, we provide an insight into the role of STING during S. aureus infection. Our data revealed that the STING signaling pathway was activated in S. aureus-infected cells. In vitro investigations demonstrated that inhibiting STING reduced inflammation, hypoxia-inducible factor-1 alpha (HIF1 alpha) expression, and mitochondrial reactive oxygen species (mROS) production. Interestingly, blocking HIF1 alpha eliminated the escalation of inflammation associated with STING. Additionally, suppressing mROS production significantly reduced HIF1 alpha expression and inflammation levels, while elevating mROS had the opposite effect. These results indicate that STING promoted inflammation through the mROS-HIF1 alpha pathway. Given that glycolysis is driven by HIF1 alpha, we investigated the role of glycolysis during infection. As expected, STING-elevated inflammation was linked with HIF1 alpha-driven glycolysis. In terms of pathogenesis, STING contributed to S. aureus proliferation within cells and mouse mammary glands. Collectively, our findings demonstrate that STING facilitates infection via the mROS-HIF1 alpha-glycolysis axis, highlighting its potential as a promising anti-inflammatory target.

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