Basic fibroblast growth factor(FGF2) plays a crucial role in influenza A virus-induced acute lung injury through neutrophil recruitment
作者单位：State Key Laboratory of Pathogens and Biosecurity Beijing Institute of Microbiology and Epidemiology 中国人民解放军第三〇二医院
会议名称：《中国生物工程学会第二届青年科技论坛暨首届青年工作委员会学术年会》
会议日期：2017年
学科分类：1007[医学-药学(可授医学、理学学位)] 100705[医学-微生物与生化药学] 1001[医学-基础医学(可授医学、理学学位)] 100103[医学-病原生物学] 10[医学]
关 键 词：H1N1 FGF2 neutrophils NFκB signaling therapy
摘 要：Influenza virus(IFV) infection is a major cause of severe respiratory illness that affects almost every country in the world. IFV infections result in respiratory illness and even acute lung injury and death, but the underlying mechanisms responsible for IFV pathogenesis remain to be fully elucidated. In this study, we found that the basic fibroblast growth factor2(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-NFκB signaling pathway. FGF2 depletion or knockout exacerbated influenza-associated disease by impairing neutrophil recruitment and activation. More importantly, administration of recombinant FGF2 protein significantly alleviated the severity of IFV-induced lung injury and promoted the survival of IFV-infected animals that was mediated by the recruited neutrophils. These findings demonstrate that FGF2 plays a critical role in preventing IFV-induced lung injury and suggest FGF2 as a promising potential therapeutic target during IFV infection.