Xie Qingqing, Liu Lele, Zhang Ziwei, Li Yanfeng, Qi Xiaopeng, Xu Tao, Xu Xiaoqing
Key Laboratory for Experimental Teratology of the Ministry of Education, Advanced Medical Research Institute, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Department of Virology, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Biochem Biophys Rep. 2025 Aug 26;44:102213. doi: 10.1016/j.bbrep.2025.102213. eCollection 2025 Dec.
Multidrug-resistant , a prevalent opportunistic pathogen in hospitals, presents a substantial risk to immunocompromised patients, triggering life-threatening conditions including pneumonia, bacteremia, and sepsis, which can be fatal. Therefore, it is urgent to develop new therapeutic strategies to combat and eradicate multidrug-resistant infection. Our finding reveals that promotes the mice treated with 5-fluorouracil (5-FU) to defend against multidrug-resistant infection via the mTORC1-IFN-I signaling pathway. Mechanistically, triggers mTORC1 activation through the phosphorylation of p38 MAPK, and mTORC1 is required for the subsequent activation of IFN-I signaling pathways in response to treatment. studies have demonstrated that enhances the clearance of in mice subjected to 5-FU chemotherapy, with this effect being mediated through the mTORC1 signaling pathway. Our study provides insight into the therapeutic intervention of enhancing IFN-I signaling and boosting host defense against bacterial infections via the administration of .
耐多药菌是医院中常见的机会性病原菌，对免疫功能低下的患者构成重大风险，可引发包括肺炎、菌血症和败血症等危及生命的病症，这些病症可能是致命的。因此，迫切需要开发新的治疗策略来对抗和根除耐多药菌感染。我们的研究发现表明，[具体物质]通过mTORC1-IFN-I信号通路促进接受5-氟尿嘧啶（5-FU）治疗的小鼠抵御耐多药菌感染。从机制上讲，[具体物质]通过p38 MAPK的磷酸化触发mTORC1激活，并且mTORC1是随后响应[具体物质]治疗激活IFN-I信号通路所必需的。[相关]研究表明，[具体物质]增强了接受5-FU化疗的小鼠体内[相关细菌]的清除，这种作用是通过mTORC1信号通路介导的。我们的研究为通过施用[具体物质]增强IFN-I信号和增强宿主对细菌感染的防御的治疗干预提供了见解。
