SiO 2 prompts host defense against Acinetobacter baumannii infection by mTORC1 activation
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O2 prompts host defense against Acinetobacter baumannii infection by mTORC1 activation 1,2
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Xiaomin Guo , Chaoming Wang , Tao Xu , Lu Yang , Chaohong Liu & Xiaopeng Qi 1
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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; 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 2
Received June 24, 2020; accepted July 16, 2020; published online September 1, 2020
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 SiO2 and found SiO2 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 SiO2-mediated host defense. SiO2 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. SiO2, mTORC1, host defense, Acinetobacter baumannii Citation:
Guo, X., Wang, C., Xu, T., Yang, L., Liu, C., and Qi, X. (2020). SiO2 prompts host defense against Acinetobacter baumannii infection by mTORC1 activation. Sci China Life Sci 63, https://doi.org/10.1007/s11427-020-1781-8
INTRODUCTION Chronic exposure to silica particles can cause silicosis, and silica-induced pulmonary inflammation and fibrosis in animals is a widely used model to study chronic pulmonary inflammation and fibrosis (Cohen et al., 2008; Park et al., 2015; Thakur et al., 2009). Occupational exposure to silica dust is a major risk factor for chronic obstructive pulmonary disease (COPD) (Cullinan, 2012; Hnizdo and Vallyathan, 2003). COPD is a leading cause of morbidity and mortality in both developed and developing countries. Epidemiologic and experimental evidence indicates that in addition to cigarette smoking, occupational exposure to dusts is an established risk factor for developing COPD and that
approximately 15% of all cases of COPD are work related (Boschetto et al., 2006; Cho et al., 2015). Exacerbations are considered detrimental events in the course of COPD, and bacterial or viral infections play major roles in the pathogenesis of COPD and are linked with exacerbations of COPD (Sethi, 2010; Sethi and Murphy, 2008). Growing clinical evidence
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