IL-17 selectively down-regulates TNF-alpha-induced RANTES gene expression in human colonic subepithelial myofibroblasts

J Immunol. 2002 Aug 15;169(4):1683-7. doi: 10.4049/jimmunol.169.4.1683.

Abstract

IL-17 enhances the TNF-alpha-induced IL-6 and IL-8 secretion in human colonic subepithelial myofibroblasts. In this study, we investigated how IL-17 modulates RANTES secretion in these cells. TNF-alpha potently induced RANTES secretion, but IL-17 dose-dependently inhibited the TNF-alpha-induced RANTES secretion. This was also observed at the mRNA level. Even after pretreatment with TNF-alpha for 12 h, the inhibitory effect of IL-17 was detectable. IL-17 did not affect the TNF-alpha-induced stability of the RANTES gene. IL-17 significantly decreased the TNF-alpha-induced increase in RANTES promoter activity, and IL-17 actually blocked the TNF-alpha-induced RANTES gene transcription. EMSAs demonstrated that IL-17 did not modulate the TNF-alpha-induced NF-kappaB DNA-binding activity, but markedly decreased TNF-alpha-induced IFN regulatory factor-1 (IRF-1) DNA-binding activity. Because cooperation between NF-kappaB and IRF-1 is important in the TNF-alpha-induced RANTES gene expression, the major mechanism mediating the inhibitory effect of IL-17 may be achieved by the inhibition of IRF-1 DNA-binding activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Cells, Cultured
  • Chemokine CCL5 / genetics*
  • Chemokine CCL5 / metabolism
  • Colon / cytology
  • Colon / drug effects*
  • Colon / immunology*
  • Colon / metabolism
  • DNA / genetics
  • DNA / metabolism
  • DNA-Binding Proteins / metabolism
  • Down-Regulation / drug effects
  • Fibroblasts / drug effects
  • Fibroblasts / immunology
  • Fibroblasts / metabolism
  • Humans
  • Interferon Regulatory Factor-1
  • Interleukin-17 / pharmacology*
  • NF-kappa B / metabolism
  • Phosphoproteins / metabolism
  • Promoter Regions, Genetic / drug effects
  • RNA Stability
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Transcription, Genetic / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Chemokine CCL5
  • DNA-Binding Proteins
  • IRF1 protein, human
  • Interferon Regulatory Factor-1
  • Interleukin-17
  • NF-kappa B
  • Phosphoproteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • DNA