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Basic fibroblast growth factor protects against influenza A virus-induced acute lung injury by recruiting neutrophils 被引量:3
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作者 Keyu Wang Chengcai Lai +17 位作者 tieling li Cheng Wang Wei Wang Bing Ni Changqing Bai Shaogeng Zhang lina Han Hongjing Gu Zhongpeng Zhao Yueqiang Duan Xiaolan Yang li Xing lingna Zhao Shanshan Zhou Min Xia Chengyu Jiang Xiliang Wang Penghui Yang 《Journal of Molecular Cell Biology》 SCIE CAS CSCD 2018年第6期573-585,共13页
Influenza virus (IAV)infection is a major cause of severe respiratory illness that affects almost every country in the world.IAV infections result in respiratory illness and even acute lung injury and death,but the un... Influenza virus (IAV)infection is a major cause of severe respiratory illness that affects almost every country in the world.IAV infections result in respiratory illness and even acute lung injury and death,but the underlying mechanisms responsible for IAV pathogenesis have not yet been fully elucidated.In this study,the basic fibroblast growth factor 2 (FGF2)level was markedly increased in H1N1 virus-infected humans and mice.FGF2,which is predominately derived from epithelial cells,recruits and activates neutrophils via the FGFR2-PI3K-AKT-NFKB signaling pathway.FGF2 depletion or knockout exacerbated influenzaassociated disease by impairing neutrophil recruitment and activation.More importantly,administration of the recombinant FGF2 protein significantly aUeviated the severity of IAV-induced lung injury and promoted the survival of IAV-infected mice.Based on the results from experiments in which neutrophils were depleted and adoptively transferred,FGF2 protected mice against IAV , infection by recruiting neutrophils.Thus,FGF2 plays a critical role in preventing IAV-induced lung injury,and FGF2 is a promising potential therapeutic target during IAV infection. 展开更多
关键词 influenza H1N1 virus recombinant FGF2 protein neutrophil recruitment FGFR2-PI3K-AKT-NFκB signaling therapeutic target
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