tetano
Editor, Senior Moderator
Int Immunopharmacol. 2019 Jul 6;74:105737. doi: 10.1016/j.intimp.2019.105737. [Epub ahead of print]
[h=1]Autophagy is involved in the acute lung injury induced by H9N2 influenza virus.[/h] Zhang RH[SUP]1[/SUP], Zhang HL[SUP]2[/SUP], Li PY[SUP]3[/SUP], Gao JP[SUP]3[/SUP], Luo Q[SUP]3[/SUP], Liang T[SUP]3[/SUP], Wang XJ[SUP]4[/SUP], Hao YQ[SUP]5[/SUP], Xu T[SUP]6[/SUP], Li CH[SUP]3[/SUP], Wang CL[SUP]3[/SUP], Zhang HC[SUP]7[/SUP], Xu MJ[SUP]3[/SUP], Tian SF[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus usually leads to economic loss to breeding farms and pose a serious threat to human health. Virus infecting tissues directly and influenza virus-induced excessive production of inflammatory factors play the key role in pathogenesis of the disease, but the mechanism is not well clarified. Here, the role of autophagy was investigated in H9N2 influenza virus-triggered inflammation. The results showed that autophagy was induced by H9N2 virus in A549 cells and in mice. Inhibiting autophagy by an autophagy inhibitor (3-methyladenine, 3-MA) or knockdown of Atg5(autophagy-related gene) by Atg5 siRNA significantly suppressed H9N2 virus replication, H9N2 virus-triggered inflammatory cytokines and chemokines, including IL-1β, TNF-α, IL-8, and CCL5 in vitro and in vivo, and suppressed H9N2 virus-triggered acute lung injury as indicated as accumulative mortality of mice, inflammatory cellular infiltrate and interstitial edema, thickening of the alveolar walls in mice lung tissues, increased inflammatory cytokines and chemokines, increased W/D ratio in mice. Moreover, autophagy mediated inflammatory responses through Akt-mTOR, NF-κB and MAPKs signaling pathways. Our data showed that autophagy was essential in H9N2 influenza virus-triggered inflammatory responses, and autophagy could be target to treat influenza virus-caused lung inflammation.
Copyright ? 2019 Elsevier B.V. All rights reserved.
[h=4]KEYWORDS:[/h] Acute lung injury; Autophagy; H9N2 influenza virus
PMID: 31288152 DOI: 10.1016/j.intimp.2019.105737
[h=1]Autophagy is involved in the acute lung injury induced by H9N2 influenza virus.[/h] Zhang RH[SUP]1[/SUP], Zhang HL[SUP]2[/SUP], Li PY[SUP]3[/SUP], Gao JP[SUP]3[/SUP], Luo Q[SUP]3[/SUP], Liang T[SUP]3[/SUP], Wang XJ[SUP]4[/SUP], Hao YQ[SUP]5[/SUP], Xu T[SUP]6[/SUP], Li CH[SUP]3[/SUP], Wang CL[SUP]3[/SUP], Zhang HC[SUP]7[/SUP], Xu MJ[SUP]3[/SUP], Tian SF[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza A virus usually leads to economic loss to breeding farms and pose a serious threat to human health. Virus infecting tissues directly and influenza virus-induced excessive production of inflammatory factors play the key role in pathogenesis of the disease, but the mechanism is not well clarified. Here, the role of autophagy was investigated in H9N2 influenza virus-triggered inflammation. The results showed that autophagy was induced by H9N2 virus in A549 cells and in mice. Inhibiting autophagy by an autophagy inhibitor (3-methyladenine, 3-MA) or knockdown of Atg5(autophagy-related gene) by Atg5 siRNA significantly suppressed H9N2 virus replication, H9N2 virus-triggered inflammatory cytokines and chemokines, including IL-1β, TNF-α, IL-8, and CCL5 in vitro and in vivo, and suppressed H9N2 virus-triggered acute lung injury as indicated as accumulative mortality of mice, inflammatory cellular infiltrate and interstitial edema, thickening of the alveolar walls in mice lung tissues, increased inflammatory cytokines and chemokines, increased W/D ratio in mice. Moreover, autophagy mediated inflammatory responses through Akt-mTOR, NF-κB and MAPKs signaling pathways. Our data showed that autophagy was essential in H9N2 influenza virus-triggered inflammatory responses, and autophagy could be target to treat influenza virus-caused lung inflammation.
Copyright ? 2019 Elsevier B.V. All rights reserved.
[h=4]KEYWORDS:[/h] Acute lung injury; Autophagy; H9N2 influenza virus
PMID: 31288152 DOI: 10.1016/j.intimp.2019.105737