Elsevier

Virology

Volume 345, Issue 1, 5 February 2006, Pages 96-104
Virology

TNF-α and IFN-α enhance influenza-A-virus-induced chemokine gene expression in human A549 lung epithelial cells

https://doi.org/10.1016/j.virol.2005.09.043Get rights and content
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Abstract

Lung epithelial cells are the primary cellular targets for respiratory virus pathogens such as influenza and parainfluenza viruses. Here, we have analyzed influenza A, influenza B and Sendai virus-induced chemokine response in human A549 lung epithelial cells. Influenza virus infection resulted in low CCL2/MCP-1, CCL5/RANTES, CXCL8/IL-8 and CXCL10/IP-10 production at late times of infection. However, when cells were pretreated with TNF-α or IFN-α, influenza-A-virus-induced chemokine production was greatly enhanced. Cytokine pretreatment resulted in enhanced expression of RIG-I, IKKε, interferon regulatory factor (IRF)1, IRF7 and p50 proteins. Most importantly, influenza-A-virus-induced DNA binding of IRF1, IRF3, IRF7 and NF-κB onto CXCL10 ISRE and NF-κB elements, respectively, was markedly enhanced in cytokine-pretreated cells. Our results suggest that IFN-α and TNF-α have a significant role in priming epithelial cells for higher cytokine and chemokine production in influenza A virus infection.

Keywords

Influenza virus
Chemokine
Interferon regulatory factor

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