tetano
Editor, Senior Moderator
J Mol Cell Biol. 2017 Nov 7. doi: 10.1093/jmcb/mjx047. [Epub ahead of print]
[h=1]Basic fibroblast growth factor protects against influenza A virus-induced acute lung injury by recruiting neutrophils.[/h] Wang K[SUP]1[/SUP], Lai C[SUP]1[/SUP], Li T[SUP]2[/SUP], Wang C[SUP]2[/SUP], Wang W[SUP]3[/SUP], Ni B[SUP]4[/SUP], Bai C[SUP]5[/SUP], Zhang S[SUP]6[/SUP], Han L[SUP]2[/SUP], Gu H[SUP]1[/SUP], Zhao Z[SUP]1[/SUP], Duan Y[SUP]1[/SUP], Yang X[SUP]1[/SUP], Xing L[SUP]1[/SUP], Zhao L[SUP]1[/SUP], Zhou S[SUP]1[/SUP], Xia M[SUP]1[/SUP], Jiang C[SUP]3[/SUP], Wang X[SUP]1[/SUP], Yang P[SUP]1,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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 influenza-associated disease by impairing neutrophil recruitment and activation. More importantly, administration of the recombinant FGF2 protein significantly alleviated 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.
? The Author (2017). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS. All rights reserved.
[h=4]KEYWORDS:[/h] AKT; FGFR2; NFκB signaling; PI3K; influenza H1N1 virus; neutrophil recruitment; recombinant FGF2 protein; therapeutic target
PMID: 29121325 DOI: 10.1093/jmcb/mjx047
[h=1]Basic fibroblast growth factor protects against influenza A virus-induced acute lung injury by recruiting neutrophils.[/h] Wang K[SUP]1[/SUP], Lai C[SUP]1[/SUP], Li T[SUP]2[/SUP], Wang C[SUP]2[/SUP], Wang W[SUP]3[/SUP], Ni B[SUP]4[/SUP], Bai C[SUP]5[/SUP], Zhang S[SUP]6[/SUP], Han L[SUP]2[/SUP], Gu H[SUP]1[/SUP], Zhao Z[SUP]1[/SUP], Duan Y[SUP]1[/SUP], Yang X[SUP]1[/SUP], Xing L[SUP]1[/SUP], Zhao L[SUP]1[/SUP], Zhou S[SUP]1[/SUP], Xia M[SUP]1[/SUP], Jiang C[SUP]3[/SUP], Wang X[SUP]1[/SUP], Yang P[SUP]1,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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 influenza-associated disease by impairing neutrophil recruitment and activation. More importantly, administration of the recombinant FGF2 protein significantly alleviated 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.
? The Author (2017). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS. All rights reserved.
[h=4]KEYWORDS:[/h] AKT; FGFR2; NFκB signaling; PI3K; influenza H1N1 virus; neutrophil recruitment; recombinant FGF2 protein; therapeutic target
PMID: 29121325 DOI: 10.1093/jmcb/mjx047