Basic fibroblast growth factor protects against influenza A virus-induced acute lung injury by recruiting neutrophils

• 来源期刊: 分子细胞生物学报（英文版）
• 年，卷（期）: 2018,（6）
• 页码范围: 573-585
• 页数: 13页
• 语种: 英文
• DOI: 10.1093/jmcb/mjx047

摘要

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-NFκB signaling pathway.FGF2 depletion or knockout exacerbated influenzaassociated disease by impairing neutrophil recruitment and activation.More importantly,administration of the recombinant FGF2 protein significantly alleviated the severity of lAY-induced lung injury and promoted the survival of lAY-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 lAY-induced lung injury,and FGF2 is a promising potential therapeutic target during IAV infection.