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Am J Physiol Lung Cell Mol Physiol 287: L1048-L1055, 2004. First published July 23, 2004; doi:10.1152/ajplung.00396.2003
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Exaggerated IL-8 and IL-6 responses to TNF-{alpha} by parainfluenza virus type 4-infected NCI-H292 cells

Thierry Roger,1,2 Paul Bresser,1 Mieke Snoek,2 Koen van der Sluijs,1,2,3 Arjen van den Berg,1,2 Monique Nijhuis,4 Henk M. Jansen,1 and René Lutter1,2

1Department of Pulmonology, 2Laboratory of Experimental Immunology, and 3Department of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, 1100 DE Amsterdam; and 4Eijkman-Winkler Institute, Department of Virology, University Medical Center, 3508 GA Utrecht, The Netherlands

Submitted 19 November 2003 ; accepted in final form 20 July 2004

Respiratory viruses induce and potentiate airway inflammation, which is related to the induction of proinflammatory mediators such as interleukin (IL)-8 and IL-6. Here we report on mechanisms implicated in IL-8 and IL-6 production by airway epithelium-like NCI-H292 cells exposed to parainfluenza virus type 4a (PIV-4). PIV-4 readily infected NCI-H292 cells as reflected by intracellular PIV-4 antigen expression. PIV-4 infection triggered a biphasic IL-8 and IL-6 mRNA response. Transient transfection with truncated and mutated promoter constructs identified NF-{kappa}B and activator protein (AP)-1, and CCAAT-enhancer binding protein (C/EBP) as the relevant transcription factors for PIV-4-induced IL-8 and IL-6 gene transcription, respectively. An increase of DNA-binding activities for NF-{kappa}B and C/EBP paralleled the induction of the first and second IL-8 and IL-6 mRNA peaks, whereas the onset of AP-1 paralleled the first IL-8 mRNA peak only. The second mRNA peak, apparently dependent on viral replication, coincided also with a marked reduction of IL-8 and IL-6 mRNA degradation. Importantly, cells at the time of the reduced mRNA degradation displayed an exaggerated IL-8 and IL-6 protein production to a secondary stimulus, as exemplified by steeper dose-response curves to TNF-{alpha}. Thus PIV-4 infection enhances epithelial IL-8 and IL-6 production by transcriptional and posttranscriptional mechanisms. The previously unrecognized phase of reduced IL-8 and IL-6 mRNA degradation and the concurrent amplified epithelial IL-8 and IL-6 responses may play an important role in virus-induced potentiation of airway inflammation.

inflammation; exacerbation; mRNA degradation; airway epithelium


Address for reprint requests and other correspondence: R. Lutter, Dept. of Pulmonology/Lab. of Experimental Immunology, G1-140, Academic Medical Center, Meibergdreef 9, PO Box 22700, 1100 DE Amsterdam, The Netherlands (E-mail: r.lutter{at}amc.uva.nl)




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