Incomplete regulation of NF-κB by IκBα during respiratory syncytial virus infection in A549 cells

MA Fiedler, K Wernke-Dollries - Journal of virology, 1999 - Am Soc Microbiol
MA Fiedler, K Wernke-Dollries
Journal of virology, 1999Am Soc Microbiol
Respiratory syncytial virus (RSV) infection of airway epithelial cells results in persistent NF-
κB activation and NF-κB-mediated interleukin-8 production. Previous studies in airway
epithelial cells demonstrated that tumor necrosis factor alpha (TNF-α)-induced NF-κB
activation is transient due to regulation by IκBα. However, during RSV infection, IκBα has
only a partial inhibitory effect on NF-κB activation. Studies presented here demonstrate that
neither increased IκBα production which occurs as a result of RSV-induced NF-κB activation …
Abstract
Respiratory syncytial virus (RSV) infection of airway epithelial cells results in persistent NF-κB activation and NF-κB-mediated interleukin-8 production. Previous studies in airway epithelial cells demonstrated that tumor necrosis factor alpha (TNF-α)-induced NF-κB activation is transient due to regulation by IκBα. However, during RSV infection, IκBα has only a partial inhibitory effect on NF-κB activation. Studies presented here demonstrate that neither increased IκBα production which occurs as a result of RSV-induced NF-κB activation nor inhibition of proteasome-mediated IκBα degradation results in a reversal of RSV-induced NF-κB activation. Thus, while manipulation of IκBα results in reversal of TNF-α-induced NF-κB activation, manipulation of IκBα does not result in a reversal of RSV-induced NF-κB activation.
American Society for Microbiology