Respiratory syncytial virus increases IL-8 gene expression and protein release in A549 cells

Am J Physiol. 1995 Dec;269(6 Pt 1):L865-72. doi: 10.1152/ajplung.1995.269.6.L865.


The mechanism of respiratory syncytial virus (RSV)-induced inflammation in the airways of infants and children is not fully understood. We hypothesized that RSV directly induces interleukin (IL)-8 gene expression in airway epithelial cells, independent of IL-1 beta and tumor necrosis factor-alpha (TNF-alpha) production. Exposure of A549 cells (an airway epithelial cell line) to RSV resulted in increased IL-8 mRNA expression and IL-8 protein release from the cells as early as 2 h after treatment. Neither IL-1 beta nor TNF-alpha (mRNA or protein) were detected. Viral replication was not necessary for the effects of RSV on IL-8 mRNA expression and protein release early in the infectious process. However, sustained levels of increased IL-8 production required RSV replication. A dose-response relationship was observed between the multiplicity of infection and IL-8 production with both active and nonreplicative RSV at the 2-h time point. Both active RSV and nonreplicative RSV increased the transcriptional activity of the 1.6-kb 5' flanking region of the IL-8 gene. Neither active RSV nor nonreplicative RSV increased the stability of the IL-8 mRNA in A549 cells. We conclude that RSV increases IL-8 gene expression in A549 cells in a biphasic pattern independent of viral replication early (2 h) but dependent on viral replication late (24 h).

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Chlorocebus aethiops
  • Drug Stability
  • Gene Expression*
  • Genes
  • Humans
  • Interleukin-8 / genetics*
  • Interleukin-8 / metabolism*
  • Lung Neoplasms / metabolism*
  • Lung Neoplasms / pathology
  • RNA, Messenger / metabolism
  • Respiratory Syncytial Virus Infections / metabolism
  • Respiratory Syncytial Viruses / growth & development
  • Respiratory Syncytial Viruses / physiology*
  • Time Factors
  • Transcription, Genetic
  • Tumor Cells, Cultured
  • Virus Replication


  • Interleukin-8
  • RNA, Messenger