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Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-kappa B and p38 MAPK signaling pathways

文献类型：期刊论文

作者Pan, Hong1; Zhang, Yijuan1; Luo, Zichao1; Li, Ping1; Liu, Lanlan1; Wang, Ce1; Wang, Hanzhong2,3; Li, Hongchang1; Ma, Yifan1
刊名AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
出版日期2014
卷号306期号:2页码:L183-L195
关键词avian influenza H5N1 virus autophagy lung inflammation NF-kappa B p38 MAPK
ISSN号1040-0605
DOI10.1152/ajplung.00147.2013
英文摘要Since avian influenza virus H5N1-induced hypercytokemia plays a key role in acute lung injury, understanding its molecular mechanism is highly desirable for discovering therapeutic targets against H5N1 infection. In the present study, we investigated the role of autophagy in H5N1-induced lung inflammation by using H5N1 pseudotyped viral particles (H5N1pps). The results showed that H5N1pps significantly induced autophagy both in A549 human lung epithelial cells and in mouse lung tissues, which was primarily due to hemagglutinin (HA) of H5N1 virus. Blocking autophagy with 3-methyladenine (an autophagy inhibitor) or siRNA knockdown of autophagy-related genes (beclin1 and atg5) dramatically attenuated H5N1pp-induced proinflammatory cytokines and chemokines, such as IL-1 beta, TNF-alpha, IL-6, CCL2, and CCL5, both in vitro and in vivo. Autophagy-mediated inflammatory responses involved the activation of NF-kappa B and p38 MAPK signaling pathways, which required the presence of clathrin but did not rely on p62 or autophagosome-lysosome fusion. On the other hand, the activation of NF-kappa B also promoted H5N1pp-induced autophagosome formation. These data indicated a positive feedback loop between autophagy and NF-kappa B signaling cascade, which could exacerbate H5N1pp-induced lung inflammation. Our data demonstrated an essential role of autophagy in H5N1pp-triggered inflammatory responses, and targeting the autophagic pathway could be a promising strategy to treat H5N1 virus-caused lung inflammation.
资助项目National Basic Research Program of China (973 Program)[2011CB933600] ; National Natural Science Foundation of China[81171446] ; Shenzhen Basic Research Program[JC201005260247A] ; Guangdong Innovation Research Team Fund for LowCost Healthcare Technologies (GIRTF-LCHT) ; Science and Technology Program of Guangdong Province[2012B090400043] ; Science and Technology Program of Guangdong Province[2012B090600036]
WOS研究方向Physiology ; Respiratory System
语种英语
WOS记录号WOS:000329858000008
出版者AMER PHYSIOLOGICAL SOC
源URL[http://202.127.146.157/handle/2RYDP1HH/3919]  
专题中国科学院武汉植物园
通讯作者Ma, Yifan
作者单位1.Chinese Acad Sci, Shenzhen Inst Adv Technol, Shenzhen Innovat Pharmacol & Biotherapy Pre clin, Guangdong Key Lab Nanomed,Key Lab Hlth Informat, Shenzhen, Peoples R China
2.Wuhan Inst Virol, State Key Lab Virol, Wuhan, Peoples R China
3.Chinese Acad Sci, Wuhan, Peoples R China
推荐引用方式
GB/T 7714		 Pan, Hong,Zhang, Yijuan,Luo, Zichao,et al. Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-kappa B and p38 MAPK signaling pathways[J]. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,2014,306(2):L183-L195.
APA Pan, Hong.,Zhang, Yijuan.,Luo, Zichao.,Li, Ping.,Liu, Lanlan.,...&Ma, Yifan.(2014).Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-kappa B and p38 MAPK signaling pathways.AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY,306(2),L183-L195.
MLA Pan, Hong,et al."Autophagy mediates avian influenza H5N1 pseudotyped particle-induced lung inflammation through NF-kappa B and p38 MAPK signaling pathways".AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY 306.2(2014):L183-L195.

入库方式： OAI收割

来源：武汉植物园

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