Dexamethasone inhibits IL-12p40 production in lipopolysaccharide-stimulated human monocytic cells by down-regulating the activity of c-Jun N-terminal kinase, the activation protein-1, and NF-kappa B transcription factors

J Immunol. 2004 Jan 1;172(1):318-30. doi: 10.4049/jimmunol.172.1.318.

Abstract

IL-12 plays a critical role in the development of cell-mediated immune responses and in the pathogenesis of inflammatory and autoimmune disorders. Dexamethasone (DXM), an anti-inflammatory glucocorticoid, has been shown to inhibit IL-12p40 production in LPS-stimulated monocytic cells. In this study, we investigated the molecular mechanism by which DXM inhibits IL-12p40 production by studying the role of the mitogen-activated protein kinases (MAPKs), and the key transcription factors involved in human IL-12p40 production in LPS-stimulated monocytic cells. A role for c-Jun N-terminal kinase (JNK) MAPK in LPS-induced IL-12p40 regulation in a promonocytic THP-1/CD14 cell line was demonstrated by using specific inhibitors of JNK activation, SP600125 and a dominant-negative stress-activated protein/extracellular signal-regulated kinase kinase-1 mutant. To identify transcription factors regulating IL-12p40 gene transcription, extensive deletion analyses of the IL-12p40 promoter was performed. The results revealed the involvement of a sequence encompassing the AP-1-binding site, in addition to that of NF-kappaB. The role of AP-1 in IL-12p40 transcription was confirmed by using antisense c-fos and c-jun oligonucleotides. Studies conducted to understand the regulation of AP-1 and NF-kappaB activation by JNK MAPK revealed that both DXM and SP600125 inhibited IL-12p40 gene transcription by inhibiting the activation of AP-1 and NF-kappaB transcription factors as revealed by luciferase reporter and gel mobility shift assays. Taken together, our results suggest that DXM may inhibit IL-12p40 production in LPS-stimulated human monocytic cells by down-regulating the activation of JNK MAPK, the AP-1, and NF-kappaB transcription factors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Anthracenes / pharmacology
  • Base Sequence
  • Binding, Competitive / drug effects
  • Binding, Competitive / genetics
  • Binding, Competitive / immunology
  • Cell Line, Tumor
  • Dexamethasone / pharmacology*
  • Down-Regulation / drug effects*
  • Down-Regulation / immunology
  • Enzyme Activation / drug effects
  • Enzyme Activation / immunology
  • Enzyme Inhibitors / pharmacology
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Interleukin-12 / antagonists & inhibitors*
  • Interleukin-12 / biosynthesis
  • Interleukin-12 / genetics
  • Interleukin-12 / physiology
  • Interleukin-12 Subunit p40
  • JNK Mitogen-Activated Protein Kinases
  • Lipopolysaccharide Receptors / biosynthesis
  • Lipopolysaccharides / pharmacology*
  • Macrophage Activation / drug effects
  • Macrophage Activation / immunology
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors*
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / metabolism
  • Mitogen-Activated Protein Kinases / physiology
  • Molecular Sequence Data
  • Monocytes / drug effects
  • Monocytes / enzymology
  • Monocytes / immunology*
  • Monocytes / metabolism
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / metabolism
  • Oligonucleotides, Antisense / pharmacology
  • Promoter Regions, Genetic
  • Protein Binding / drug effects
  • Protein Binding / genetics
  • Protein Binding / immunology
  • Protein Subunits / antagonists & inhibitors*
  • Protein Subunits / biosynthesis
  • Protein Subunits / genetics
  • Protein Subunits / physiology
  • Proto-Oncogene Proteins c-fos / genetics
  • Transcription Factor AP-1 / antagonists & inhibitors*
  • Transcription Factor AP-1 / metabolism
  • Transcription, Genetic
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Anthracenes
  • Enzyme Inhibitors
  • Immunosuppressive Agents
  • Interleukin-12 Subunit p40
  • Lipopolysaccharide Receptors
  • Lipopolysaccharides
  • NF-kappa B
  • Oligonucleotides, Antisense
  • Protein Subunits
  • Proto-Oncogene Proteins c-fos
  • Transcription Factor AP-1
  • Interleukin-12
  • pyrazolanthrone
  • Dexamethasone
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases