tetano
Editor, Senior Moderator
Oncotarget. 2017 Mar 8. doi: 10.18632/oncotarget.16016. [Epub ahead of print]
[h=1]RIP3 deficiency ameliorates inflammatory response in mice infected with influenza H7N9 virus infection.[/h] Xu YL[SUP]1[/SUP], Tang HL[SUP]1[/SUP], Peng HR[SUP]1[/SUP], Zhao P[SUP]1[/SUP], Qi ZT[SUP]1[/SUP], Wang W[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza H7N9 virus infection causes an acute, highly contagious respiratory illness that triggers cell death of infected cells and airway epithelial destruction. RIP3 is a key regulator of cell death responses to a growing number of viral and microbial agents. This study aimed to investigate the role of RIP3 in inflammation of influenza H7N9 virus infection. Here, RIP3 knock out (RIP3-/-) mice and littermate wild type mice were infected intranasally with influenza H7N9 virus (A/Fujian/S03/2015) to determine the contribution of RIP3 to the inflammatory response of influenza H7N9 virus infection. It was found that RIP3-/- mice infected with H7N9 virus showed higher survival and less weight loss, compared with wild type littermate mice. In addition, RIP3-/- mice had fewer regions of edema, infiltration with inflammatory cells, and alvelolar collapses, and the secretions of IL-1β, IL-6, RANTES and MIP-1 in BALF were significantly decreased on days 3 and 7 p.i. when compared with WT mice. Moreover, caspase 1/IL1β signaling was found to be invovled in RIP3 associated imflammation of influenza H7N9 virus, but not RIP3/MLKL dependent necrosis. In the conclusion, our results indicated that RIP3 deficiency can protect mice from the infection of influenza H7N9 virus by downregulating caspase 1/IL1β signaling, which provided edivence of the RIP3 invovled necroptosis independent manner.
[h=4]KEYWORDS:[/h] H7N9 virus; Immune response; Immunity; Immunology and Microbiology Section; RIP3; influenza A virus; necroptosis; proinflammatory cytokines
PMID: 28423682 DOI: 10.18632/oncotarget.16016
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[h=1]RIP3 deficiency ameliorates inflammatory response in mice infected with influenza H7N9 virus infection.[/h] Xu YL[SUP]1[/SUP], Tang HL[SUP]1[/SUP], Peng HR[SUP]1[/SUP], Zhao P[SUP]1[/SUP], Qi ZT[SUP]1[/SUP], Wang W[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Influenza H7N9 virus infection causes an acute, highly contagious respiratory illness that triggers cell death of infected cells and airway epithelial destruction. RIP3 is a key regulator of cell death responses to a growing number of viral and microbial agents. This study aimed to investigate the role of RIP3 in inflammation of influenza H7N9 virus infection. Here, RIP3 knock out (RIP3-/-) mice and littermate wild type mice were infected intranasally with influenza H7N9 virus (A/Fujian/S03/2015) to determine the contribution of RIP3 to the inflammatory response of influenza H7N9 virus infection. It was found that RIP3-/- mice infected with H7N9 virus showed higher survival and less weight loss, compared with wild type littermate mice. In addition, RIP3-/- mice had fewer regions of edema, infiltration with inflammatory cells, and alvelolar collapses, and the secretions of IL-1β, IL-6, RANTES and MIP-1 in BALF were significantly decreased on days 3 and 7 p.i. when compared with WT mice. Moreover, caspase 1/IL1β signaling was found to be invovled in RIP3 associated imflammation of influenza H7N9 virus, but not RIP3/MLKL dependent necrosis. In the conclusion, our results indicated that RIP3 deficiency can protect mice from the infection of influenza H7N9 virus by downregulating caspase 1/IL1β signaling, which provided edivence of the RIP3 invovled necroptosis independent manner.
[h=4]KEYWORDS:[/h] H7N9 virus; Immune response; Immunity; Immunology and Microbiology Section; RIP3; influenza A virus; necroptosis; proinflammatory cytokines
PMID: 28423682 DOI: 10.18632/oncotarget.16016
Free full text