Poly I:C and respiratory syncytial virus (RSV) inhibit glucocorticoid receptor (GR)-mediated transactivation in lung epithelial, but not monocytic, cell lines

Virus Res. 2013 Sep;176(1-2):303-6. doi: 10.1016/j.virusres.2013.06.011. Epub 2013 Jul 2.

Abstract

Respiratory syncytial virus (RSV)-induced bronchiolitis in infants is not responsive to glucocorticoids. We have recently shown that RSV infection of lung epithelial cells impairs glucocorticoid receptor (GR) function. In this current study, we have shown that the viral mimic poly I:C also represses GR-mediated gene activation in lung epithelial cells, suggesting that this might be a common phenomenon of other viral infections. However, we also show that neither RSV infection nor poly I:C affect GR-mediated gene activation in the monocytic cell line THP-1, suggesting that these effects on GR function may be cell-type specific.

Keywords: Epithelial cells; Glucocorticoid receptor; Monocytes; Poly I:C; Respiratory syncytial virus.

MeSH terms

  • Cell Line
  • Cells, Cultured
  • Epithelial Cells / immunology*
  • Epithelial Cells / virology*
  • Humans
  • Infant
  • Monocytes / immunology*
  • Monocytes / virology*
  • Poly I-C / metabolism*
  • Receptors, Glucocorticoid / metabolism*
  • Respiratory Syncytial Virus, Human / growth & development*
  • Transcriptional Activation

Substances

  • Receptors, Glucocorticoid
  • Poly I-C