Reduction of IL-12 p40 production in activated monocytes after exposure to diesel exhaust particles
Autor: | R. Hagemann, Kjartan Egeberg, Anders Sundan, Asbjørn Magne Nilsen, T. Nørkov, H. Eikås |
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Rok vydání: | 2002 |
Předmět: |
Hypersensitivity
Immediate Lipopolysaccharides Allergy Diesel exhaust medicine.medical_treatment Immunology Down-Regulation complex mixtures Monocytes Cell Line Atopy medicine Immunology and Allergy Humans Particle Size Asthma Vehicle Emissions Lung business.industry Tumor Necrosis Factor-alpha General Medicine respiratory system Interleukin 12 p40 medicine.disease Interleukin-12 respiratory tract diseases Protein Subunits medicine.anatomical_structure Interleukin 12 business human activities Adjuvant |
Zdroj: | International archives of allergy and immunology. 131(3) |
ISSN: | 1018-2438 |
Popis: | 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 µg/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 µg/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. |
Databáze: | OpenAIRE |
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