Modulation of mast cell proteinase-activated receptor expression and IL-4 release by IL-12

Immunol Cell Biol. 2007 Oct;85(7):558-66. doi: 10.1038/sj.icb.7100085. Epub 2007 Jun 26.

Abstract

It has been recognized that protease-activated receptors (PARs), interleukin (IL)-4 and IL-6 are involved in the pathogenesis of allergic diseases, and that IL-12 plays a role in adaptive immune response. However, little is known of the effect of IL-12 on protease-induced cytokine release from mast cells. In the present study, we examined potential influence of IL-12 on mast cell PAR expression and IL-4 and IL-6 release. The results showed that IL-12 downregulated the expression of PAR-2 and upregulated expression of PAR-4 on P815 cells. It also downregulated expression of PAR-2 mRNA, and upregulated expression of PAR-1, PAR-3 and PAR-4 mRNAs. However, IL-12 enhanced trypsin- and tryptase-induced PAR-2 and PAR-2 mRNA expression. It was observed that IL-12 induced release of IL-4, but reduced trypsin- and tryptase-stimulated IL-4 secretion from P815 cells. PD98059, U0126 and LY294002 not only abolished IL-12-induced IL-4 release but also inhibited IL-12-induced phosphorylation of extracellular signal-regulated kinase and Akt. In conclusion, IL-12 may serve as a regulator in keeping the balance of Th1 and Th2 cytokine production in allergic inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Butadienes / pharmacology
  • Cells, Cultured
  • Chromones / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Flavonoids / pharmacology
  • Gene Expression Regulation / drug effects
  • Imidazoles / pharmacology
  • Interleukin-12 / pharmacology*
  • Interleukin-4 / metabolism*
  • Mast Cells / drug effects*
  • Mast Cells / metabolism*
  • Mice
  • Morpholines / pharmacology
  • Nitriles / pharmacology
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / metabolism
  • Pyridines / pharmacology
  • RNA, Messenger / metabolism
  • Receptors, Proteinase-Activated / genetics
  • Receptors, Proteinase-Activated / metabolism*
  • Trypsin / pharmacology
  • Tryptases / pharmacology
  • Tyrphostins / pharmacology

Substances

  • Butadienes
  • Chromones
  • Enzyme Inhibitors
  • Flavonoids
  • Imidazoles
  • Morpholines
  • Nitriles
  • Pyridines
  • RNA, Messenger
  • Receptors, Proteinase-Activated
  • Tyrphostins
  • U 0126
  • alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide
  • Interleukin-12
  • Interleukin-4
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases
  • Trypsin
  • Tryptases
  • SB 203580
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one