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作 者:Xiaomin Guo Chaoming Wang Tao Xu Lu Yang Chaohong Liu Xiaopeng Qi
机构地区:[1]Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences/Key Laboratory of Bioactive Peptides of Yunnan Province,Kunming Institute of Zoology,Chinese Academy of Sciences,Kunming 650223,China [2]Advanced Medical Research Institute,Cheeloo College of Medicine,Shandong University,Jinan 250012,China [3]Department of Pathogen Biology,School of Basic Medicine,Huazhong University of Science and Technology,Wuhan 430030,China
出 处:《Science China(Life Sciences)》2021年第6期982-990,共9页中国科学(生命科学英文版)
基 金:supported by the National Key Research and Development Program of China(2017YFD0500300);the National Natural Science Foundation of China(31970896,31701134 and 81701578);Yunnan Province(2019FJ008,2018FA038,2018FB127,2018FB131,HXDTZX-2019-1,HXDT-2019-2,and AMHD-2018-2)。
摘 要:Host-pathogen interactions in the setting of chronic pulmonary inflammation remain unclear,and the occurrence of pneumonia is increased in patients with chronic obstructive pulmonary disease who use immunosuppressive drugs.We performed Acinetobacter baumannii infection in mice with chronic pulmonary inflammation after intranasal administration of SiO_(2) and found SiO_(2) treatment increased host defense against A.baumannii infection.Innate immune responses initiated by NF-κB,type 1 interferon,NLRP3 and AIM2 inflammasomes were dispensable for SiO_(2)-mediated host defense.SiO_(2)treatment activated the mTORC1 signaling,and mTORC1 was crucial for host defense against A.baumannii infection.Our study highlights the protective role of mTORC1 signaling in host defense against bacterial infection,offers novel insights into understanding the mechanisms of immunosuppressive drug-related pneumonia,and provides potential host-directed therapeutics to treat bacterial infections.
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