Reduction of IL-12 p40 production in activated monocytes after exposure to diesel exhaust particles

Int Arch Allergy Immunol. 2003 Jul;131(3):201-8. doi: 10.1159/000071487.


Background: A reduction of IL-12 production by lung macrophages may partly explain the presumed adjuvant effect of diesel exhaust particles (DEP) in allergy and asthma. IL-12 stimulates T helper type 1 (Th1) lymphocytes, which inhibit Th2 cells via Th1-specific cytokines. The aim of this study was to investigate the influence of DEP on the production of IL-12 p40 in lipopolysaccharide (LPS)-activated monocytes.

Methods: The human monocytic cell line Mono-Mac-6 was stimulated with LPS (200 ng/ml) and grown with DEP (0-200 microg/ml) for 0, 6 or 24 h. IL-12 p40 and the pro-inflammatory cytokine TNF were analysed in the cell supernatants by ELISA and a cell assay, respectively.

Results: Levels of IL-12 p40 correlated inversely with the DEP exposure concentrations, whereas TNF increased in parallel to the DEP concentrations. At a DEP concentration of 200 microg/ml, the amount of IL-12 p40 was 35% of that observed without DEP. The corresponding TNF value was 230% of the control. Reduced viability, binding of cytokines to DEP or endotoxin in the DEP samples cannot fully explain the changes in the concentrations of these two cytokines.

Conclusion: DEP seem to inhibit the production of IL-12 p40 and stimulate that of TNF in activated monocytes. This may partly explain the presumed adjuvant effect of DEP in atopy; by altering the Th1/Th2 balance via down-regulation of IL-12, the Th2 response characteristic of allergy and asthma may be favoured.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Asthma / immunology
  • Asthma / physiopathology
  • Cell Line
  • Down-Regulation*
  • Humans
  • Hypersensitivity, Immediate / immunology
  • Hypersensitivity, Immediate / physiopathology
  • Interleukin-12 / biosynthesis*
  • Lipopolysaccharides / pharmacology
  • Monocytes / immunology*
  • Particle Size
  • Protein Subunits / biosynthesis*
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Vehicle Emissions / adverse effects*


  • Lipopolysaccharides
  • Protein Subunits
  • Tumor Necrosis Factor-alpha
  • Vehicle Emissions
  • Interleukin-12