Infection and chronic disease activate a systemic brain-muscle signaling axis

文献类型： 外文期刊

第一作者： Yang, Shuo

作者： Yang, Shuo;Yamada, Shigehiro;Ou, Tiffany;McAdow, Jennifer;Johnson, Aaron;Yang, Shuo;Wang, Rong;Tian, Meijie;Dai, Yulong;Feng, Shengyong;Cheng, Gong;Dai, Yulong;Tai, Wanbo;Cheng, Gong;Dai, Yulong;Yin, Xin;Wang, Yunyun;Chhangani, Deepak;Rincon-Limas, Diego E.;Chhangani, Deepak;Rincon-Limas, Diego E.;Chhangani, Deepak;Rincon-Limas, Diego E.;Chhangani, Deepak;Rincon-Limas, Diego E.;Li, Wenle;Li, Wenle;Guo, Xuan;Cheng, Gong;Cheng, Gong

作者机构：

期刊名称：SCIENCE IMMUNOLOGY （ 影响因子：17.6； 五年影响因子：19.1 ）

ISSN： 2470-9468

年卷期： 2024 年 9 卷 97 期

页码：

收录情况： SCI

摘要： Infections and neurodegenerative diseases induce neuroinflammation, but affected individuals often show nonneural symptoms including muscle pain and muscle fatigue. The molecular pathways by which neuroinflammation causes pathologies outside the central nervous system (CNS) are poorly understood. We developed multiple models to investigate the impact of CNS stressors on motor function and found that Escherichia coli infections and SARS-CoV-2 protein expression caused reactive oxygen species (ROS) to accumulate in the brain. ROS induced expression of the cytokine Unpaired 3 (Upd3) in Drosophila and its ortholog, IL-6, in mice. CNS-derived Upd3/IL-6 activated the JAK-STAT pathway in skeletal muscle, which caused muscle mitochondrial dysfunction and impaired motor function. We observed similar phenotypes after expressing toxic amyloid-beta (A beta 42) in the CNS. Infection and chronic disease therefore activate a systemic brain-muscle signaling axis in which CNS-derived cytokines bypass the connectome and directly regulate muscle physiology, highlighting IL-6 as a therapeutic target to treat disease-associated muscle dysfunction.

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