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Am. J. Respir. Crit. Care Med., Volume 156, Number 1, July 1997, 36-42

Diesel Exhaust Particles Enhance Antigen-induced Airway Inflammation and Local Cytokine Expression in Mice

HIROHISA TAKANO, TOSHIKAZU YOSHIKAWA, TAKAMICHI ICHINOSE, YUICHI MIYABARA, KOICHI IMAOKA, and MASARU SAGAI

Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies, Tsukuba, Ibaraki; First Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto; and the National Institute of Public Health, Tokyo, Japan

Previous experimental studies have suggested that nasal instillation of diesel exhaust particles (DEP) can enhance nasal IgE response and cytokine production. However, there is no experimental evidence for the relation of DEP to allergic asthma. We investigated the effects of DEP inoculated intratracheally on antigen-induced airway inflammation, local expression of cytokine proteins, and antigen-specific immunoglobulin production in mice. DEP aggravated ovalbumin-induced airway inflammation characterized by infiltration of eosinophils and lymphocytes and an increase in goblet cells in bronchial epithelium. DEP with antigen markedly increased interleukin-5 (IL-5) protein levels in lung tissue and bronchoalveolar lavage supernatants compared with either antigen or DEP alone. The combination of DEP and antigen induced significant increases in local expression of IL-4, granulocyte macrophage-colony stimulating factor (GM-CSF), and IL-2, whereas expression of interferon-gamma was not affected. In addition, DEP exhibited adjuvant activity for the antigen-specific production of IgG and IgE. These results provide the first experimental evidence that DEP can enhance the manifestations of allergic asthma. The enhancement may be mediated mainly by the increased local expression of IL-5, and also by the modulated expression of IL-4, GM-CSF, and IL-2.




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