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Rapamycin ameliorates lipopolysaccharide-induced acute lung injury by inhibiting IL-1 beta and IL-18 production

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资源类型：

收录情况： ◇ SCIE

作者：
Xuehong Jia[a,b] * ; Bin Cao[c,d,e] ; Yunqing An[f] ; Xulong Zhang[f] ; Chen Wang[b,c,d,e,g,*1] ;
机构： [a]Department of Respiratory Medicine, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China [b]Peking University China-Japan Friendship School of Clinical Medicine, Beijing 100029, China [c]Department of Pulmonary and Critical Care Medicine, Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing 100029, China [d]National Clinical Research Center for Respiratory Diseases, Beijing 100029, China [e]Department of Respiratory Medicine, Capital Medical University, Beijing 100069, China [f]Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China [g]Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100730, China
出处：
DOI： 10.1016/j.intimp.2018.12.017
ISSN：

关键词： Acute lung injury IL-1 beta IL-18 mTOR Autophagy NF-kappa B

摘要：
Interleukin (IL)-1 beta and IL-18 play central and detrimental roles in the development of acute lung injury (ALI), and mammalian target of rapamycin (mTOR) is involved in regulating IL-1 beta and IL-18 production. However, it is not clear whether the mTOR specific inhibitor rapamycin can attenuate lipopolysaccharide (LPS)-induced ALI by modulating IL-1 beta and IL-18 production. In this study, we found that rapamycin ameliorated LPS-induced ALI by inhibiting NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated IL-1 beta and IL-18 secretion. Mechanistically, elevated autophagy and decreased nuclear factor (NF)-kappa B activation were associated with downregulated IL-1 beta and IL-18. Moreover, rapamycin reduced leukocyte infiltration in the lung tissue and bronchoalveolar lavage fluid (BALF), and contributed to the alleviation of LPS-induced ALI. Consistently, rapamycin also significantly inhibited IL-1 beta and IL-18 production by RAW264.7 cells via increased autophagy and decreased NF-kappa B signaling in vitro. Our results demonstrated that rapamycin protects mice against LPS-induced ALI partly by inhibiting the production and secretion of IL-1 beta and IL-18. mTOR and rapamycin might represent an appropriate therapeutic target and strategy for preventing ALI induced by LPS.

基金：
National Natural Science Foundation of China, ChinaNational Natural Science Foundation of China [81373114]; National Science Grant for Distinguished Young Scholars [81425001/H0104]; National Key Technology Support Program from Ministry of Science and Technology, China [2015BA112B11]; Beijing Science and Technology Project [D151100002115004]; Beijing Municipal Natural Science Foundation, ChinaBeijing Natural Science Foundation [7182013]
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2018]版：
大类 | 3 区 医学
小类 | 3 区 免疫学 3 区 药学
最新[2023]版：
大类 | 2 区 医学
小类 | 2 区 免疫学 2 区 药学
JCR分区：
出版当年[2017]版：
Q2 PHARMACOLOGY & PHARMACY Q3 IMMUNOLOGY
最新[2023]版：
Q1 PHARMACOLOGY & PHARMACY Q2 IMMUNOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

第一作者：
第一作者机构： [a]Department of Respiratory Medicine, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China [b]Peking University China-Japan Friendship School of Clinical Medicine, Beijing 100029, China
通讯作者：
通讯机构： [b]Peking University China-Japan Friendship School of Clinical Medicine, Beijing 100029, China [c]Department of Pulmonary and Critical Care Medicine, Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing 100029, China [d]National Clinical Research Center for Respiratory Diseases, Beijing 100029, China [e]Department of Respiratory Medicine, Capital Medical University, Beijing 100069, China [f]Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China [g]Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100730, China [*1]Peking University China-Japan Friendship School of Clinical Medicine, Beijing 100029, China
推荐引用方式(GB/T 7714)：
Xuehong Jia,Bin Cao,Yunqing An,et al.Rapamycin ameliorates lipopolysaccharide-induced acute lung injury by inhibiting IL-1 beta and IL-18 production[J].INTERNATIONAL IMMUNOPHARMACOLOGY.2019,67:211-219.doi:10.1016/j.intimp.2018.12.017.
APA：
Xuehong Jia,Bin Cao,Yunqing An,Xulong Zhang&Chen Wang.(2019).Rapamycin ameliorates lipopolysaccharide-induced acute lung injury by inhibiting IL-1 beta and IL-18 production.INTERNATIONAL IMMUNOPHARMACOLOGY,67,
MLA：
Xuehong Jia,et al."Rapamycin ameliorates lipopolysaccharide-induced acute lung injury by inhibiting IL-1 beta and IL-18 production".INTERNATIONAL IMMUNOPHARMACOLOGY 67.(2019):211-219

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