TGF-β1 signaling inhibit the in vitro apoptotic, infection and stimulatory cell response induced by influenza H1N1 virus infection on A549 cells
Apoptosis; IL-1β; Inflammasome; Influenza A virus (IAV); M1 viral protein; Smad7; TGF-β1.- Virus Res
- 5
- 2021 May;297:198337.
- Human
- 抗体芯片
- 呼吸系统
- 呼吸系统
- 其它细胞
- 流感
- Bad,TRAIL R1/DR4,PON2,Bax,TRAIL R2/DR5,p21/CIP1/CDNK1A,Bcl-2,FADD,p27/Kip1,Bcl-x,Fas/TNFSF6,Phospho-p53 (S15),Pro-Caspase-3,HIF-1 alpha,Phospho-p53 (S46),Cleaved Caspase-3,HO-1/HMOX1/HSP32,Phospho-p53 (S392),Catalase,HO-2/HMOX2,Phospho-Rad17 (S635),cIAP-1,HSP27,Pro-Caspase-3,cIAP-2,HSP60,SMAC/Diablo,Claspin,HSP70,Survivin,Clusterin,HTRA2/Omi,TNF RI/TNFRSF1A,Cytochrome c,Livin,XIAP
相关货号
LXAH036-1
Abstract
Influenza A virus (IAV) infection induces host cell responses that could derive in inflammatory and apoptotic response. In this respect, in multiple pathological situations, TGF-β1 has shown anti-inflammatory effect, but its role during IAV infection is poorly understood. Interestingly, recent profiling expression studies have suggested that the TGF-β1 pathway could be functionally related to the IAV infection's host response. To gain an understanding of the involvement of TGF-β1's signaling pathway during IAV infection, we compared different apoptotic proteins such as TNFR1, Fas ligand, XIAP, cIAP, among others proteins, and pro-inflammatory elements like IL-1β in the A549 cells during IAV infection (H1N1/NC/99), with and without 1 h of pre-treatment with TGF-β1. Pre-incubation with TGF-β1 significantly inhibited apoptosis and the presence of pro-apoptotic factors. Moreover, the relative abundance of immunodetected IAV M1 protein along 24 -h post-infection period was abridged, which correlated with a disminished infectious viral progeny Additionally, caspase 1 activation and increase of IL-1β induced by IAV infection was also reduced by TGF-β1 signaling activation. Whereas IAV infection increase of Smad-7 and, as consequence, partially inhibiting Smad2/3 phosphorylation, pre-treatment with TGF-β1 blocked IAV-dependent Smad7 induction and prevented Smad2/3 signaling shutdown. All these data suggest the role of TGF-β1 signaling pathway in the control of host cell response induced by the IAV infection and identify a potential clinical target to modulate acute cell death.Keywords:Apoptosis; IL-1β; Inflammasome; Influenza A virus (IAV); M1 viral protein; Smad7; TGF-β1.
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