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Toxicological Sciences 71, 207-216 (2003)
Copyright © 2003 by the Society of Toxicology

IMMUNOTOXICOLOGY

Respiratory Exposure to Diesel Exhaust Particles Decreases the Spleen IgM Response to a T Cell-Dependent Antigen in Female B6C3F1 Mice

H.-M. Yang, L. Butterworth, A. E. Munson and B. Jean Meade1

National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, West Virginia 26505

We investigated the systemic immunotoxic potential of respiratory exposure to diesel exhaust particles (DEP) in this study. Female B6C3F1 mice (~8 weeks old) were exposed to increasing concentrations of DEP intratracheally, 3 times every two weeks, and sacrificed 2 or 4 weeks after the first exposure. The systemic toxicity and immune status in mice were evaluated. Mice exposed to DEP (1 to 15 mg/kg) showed no significant changes in body, spleen, or liver weights. Lung weights were increased in the mice exposed to 15 mg/kg DEP for 2 or 4 weeks. Except for a decreased platelet count, no significant alterations occurred in hematological parameters following DEP exposure. The number of splenic anti-sheep red blood cell (sRBC) IgM antibody-forming cells (AFC) decreased following DEP exposure for 2 weeks. This effect was less severe following 4 weeks of exposure and was only evident in the high dose group. Exposure to DEP also resulted in a significant decrease in the absolute numbers and the percentages of total spleen cells for total, CD4+, and CD8+ T cells, while the numbers of B cells and total nucleated cells in spleen were not significantly changed. The proliferative response of splenocytes to the T-cell mitogen, concanavalin A (ConA), as well as their production of IL-2 and IFN-{gamma}, was decreased dose-dependently following exposure of mice to DEP for 2 weeks, whereas proliferation was not changed in response to anti-CD3 monoclonal antibody. In summary, short-term respiratory exposure of mice to DEP resulted in systemic immunosuppression with evidence of T cell-mediated and possibly macrophage-mediated mechanisms.

Key Words: diesel exhaust particles; immunosuppression; antibody-forming cell response; respiratory exposure; cytokine modulation.


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