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Gene Expression Data from Influenza A Virus-Infected and Mock-infected A549 Human Aveolar Epithelial Carcinoma Cells with Exposure to Mouse Eosinophils.

ABSTRACT: Eosinophils are terminally differentiated granulocytes that participate in innate immunity against Influenza A Virus (IAV). Here, we investigate transcriptional changes that occur in IAV-infected human A549 aveolar epithelial carcinoma cells with and without direct or indirect exposure to mouse bone marrow-derived eosinophils (BMdEos). Global changes in the transcriptome of A549 cells due to Influenza A virus-infection and/or direct and indirect eosinophil exposure were assessed using ThermoFisher/Affymetrix Clariom™ S Human microarrays.

ORGANISM(S): Homo sapiens

PROVIDER: GSE163224 | GEO | 2021/03/31

REPOSITORIES: GEO

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Project description:Fibroblast growth factor (FGF) 2 (FGF2 or basic FGF) mediates a wide range of biological functions, such as regulating proliferation, angiogenesis, migration, differentiation and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza virus (IAV) -induced lung injury remain largely unexplored. In this study, we firstly report miR-194 expression is significantly decreased in A549 cells following influenza virus A/Beijing/501/2009 (BJ501) infection. MiR-194 directly targeting FGF2, a novel antiviral regulator, could suppress FGF2 expression both in mRNA and protein levels. Overexpression miR-194 facilitate IAV replication via negatively regulating type I IFN production, and reintroduction of FGF2 abrogates miR-194-induced effects on promoting IAV replication. On the contrary, inhibition of miR-194 alleviate IAV induced lung injury via promoting type I IFNs antiviral activities in vivo. Importantly, contrary to FGF2 activated RIG-I signaling pathway, miR-194 suppressed TBK1 and IRF3 phosphorylation. Taken together, our findings demonstrated that miR-194-FGF2 axis play a vital role in IAV-induced lung injury, and miR-194 antagonism might be as a potential therapeutic target during IAV infection. Fibroblast growth factor (FGF) 2 (FGF2 or basic FGF) mediates a wide range of biological functions, such as regulating proliferation, angiogenesis, migration, differentiation and injury repair. However, the roles of FGF2 and the underlying mechanisms of action in influenza virus (IAV) -induced lung injury remain largely unexplored. In this study, we firstly report miR-194 expression is significantly decreased in A549 cells following influenza virus A/Beijing/501/2009 (BJ501) infection. MiR-194 directly targeting FGF2, a novel antiviral regulator, could suppress FGF2 expression both in mRNA and protein levels. Overexpression miR-194 facilitate IAV replication via negatively regulating type I IFN production, and reintroduction of FGF2 abrogates miR-194-induced effects on promoting IAV replication. On the contrary, inhibition of miR-194 alleviate IAV induced lung injury via promoting type I IFNs antiviral activities in vivo. Importantly, contrary to FGF2 activated RIG-I signaling pathway, miR-194 suppressed TBK1 and IRF3 phosphorylation. Taken together, our findings demonstrated that miR-194-FGF2 axis play a vital role in IAV-induced lung injury, and miR-194 antagonism might be as a potential therapeutic target during IAV infection.

Dataset Information

Gene Expression Data from Influenza A Virus-Infected and Mock-infected A549 Human Aveolar Epithelial Carcinoma Cells with Exposure to Mouse Eosinophils.

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