Dexamethasone inhibits IL-1 and TNF activity in human lung fibroblasts without affecting IL-1 or TNF receptors

M. M. Monick, T. R. Aksamit, L. J. Geist, G. W. Hunninghake

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Interleukin (IL-1) and tumor necrosis factor (TNF) activate human lung fibroblasts through interactions with specific receptors. One effect of this interaction of IL-1 and TNF with fibroblasts is an increased production of the cytokines, IL-6 and IL-8. Dexamethasone blocks the induction of IL-6 and IL-8 by IL-1 or TNF. In these studies, we determined whether dexamethasone interferes with the upregulation of IL-6 and IL-8 by downregulating expression of the IL-1 or TNF receptor genes. Confluent lung fibroblasts were treated with medium alone (control) or medium with dexamethasone (10-6 M). Dexamethasone did not decrease the binding of IL-1 and TNF to their receptors, nor did it decrease amounts of IL-1 or TNF receptor RNA. Both IL- 1 and TNF increased release of IL-6 and IL-8 from the cells in a dose- dependent manner and dexamethasone inhibited this effect. Dexamethasone also inhibited the induction of IL-6 and IL-8 RNA by IL-1 and TNF. The studies show that dexamethasone does not block the effects of IL-1 or NTF on fibroblasts by decreasing expression of IL-1 or TNF receptors.

Original languageEnglish (US)
Pages (from-to)L33-L38
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 11-1
StatePublished - 1994


  • corticosteroid
  • cytokine
  • fibrosis

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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