Cytokine mRNA decay is accelerated by an inhibitor of p38-mitogen-activated protein kinase

Inflamm Res. 1999 Oct;48(10):533-8. doi: 10.1007/s000110050499.

Abstract

Objective: To identify the site(s) in tumor necrosis factor (TNFalpha), interleukin-6 (IL-6), and macrophage inflammatory protein-1alpha (MIP-1alpha) biosynthesis that is blocked by SB202190, a selective inhibitor of p38-mitogen activated protein kinase (p38).

Materials: Human blood monocytes isolated by centrifugal elutriation.

Methods: Monocytes were stimulated with lipopolysaccharide in the presence of 0, 0.3, 1 and 3 microM SB202190. Induced TNFalpha, IL-6, and MIP-1alpha protein and mRNA were measured by ELISA and quantitative RT-PCR, respectively. The half-lives of cytokine mRNA levels were determined following treatment of cells with actinomycin D or SB202190.

Results: SB202190 suppressed >60% of lipopolysaccharide-induced TNFalpha, IL-6, and MIP-1alpha protein and mRNA expression. Suppressed mRNA levels could be attributed to a >2 to 7-fold reduction in cytokine mRNA half-lives. In contrast, SB202190 did not destabilize mRNAs encoding interferon-induced gene 15 protein and glyceraldehyde-3-phosphate dehydrogenase.

Conclusions: Specific mRNA destabilization represents an important and novel site of action for the cytokine suppressive effects of p38 inhibitors.

MeSH terms

  • Cells, Cultured
  • Chemokine CCL3
  • Chemokine CCL4
  • Cytokines / blood
  • Cytokines / genetics*
  • Enzyme Inhibitors / blood
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation / drug effects
  • Humans
  • Imidazoles / blood
  • Imidazoles / pharmacology
  • Interleukin-6 / antagonists & inhibitors
  • Interleukin-6 / biosynthesis
  • Interleukin-6 / blood
  • Interleukin-6 / genetics
  • Kinetics
  • Lipopolysaccharides / pharmacology
  • Macrophage Inflammatory Proteins / antagonists & inhibitors
  • Macrophage Inflammatory Proteins / biosynthesis
  • Macrophage Inflammatory Proteins / blood
  • Macrophage Inflammatory Proteins / genetics
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors*
  • Mitogen-Activated Protein Kinases / blood
  • Monocytes / drug effects
  • Monocytes / metabolism
  • Pyridines / blood
  • Pyridines / pharmacology
  • RNA Stability / drug effects
  • RNA, Messenger / blood
  • RNA, Messenger / chemistry
  • RNA, Messenger / drug effects*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / genetics
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Chemokine CCL3
  • Chemokine CCL4
  • Cytokines
  • Enzyme Inhibitors
  • Imidazoles
  • Interleukin-6
  • Lipopolysaccharides
  • Macrophage Inflammatory Proteins
  • Pyridines
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole