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ToxSci Advance Access published online on December 2, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfh035
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received September 11, 2003; accepted October 31, 2003
© 2003 Society of Toxicology

Environmental Toxicology

Suppression of Cell-Mediated Immune Responses to Listeria Infection by Repeated Exposure to Diesel Exhaust Particles in Brown Norway Rats

Xuejun J. Yin 1, Caroline C. Dong 1, Jane Y. C. Ma 2, James Antonini 2, Jenny R. Roberts 2, Charles F. Stanley 3, Rosana Schafer 4, and Joseph K. H. Ma 1*

1 School of Pharmacy, West Virginia University, Morgantown, West Virginia 26506, USA
2 Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA
3 Mechanical and Aerospace Engineering Department, West Virginia University, Morgantown, West Virginia 26506, USA
4 School of Medicine, West Virginia University, Morgantown, West Virginia 26506, USA

* To whom correspondence should be addressed. E-mail: jma{at}hsc.wvu.edu.


  Abstract

Diesel exhaust particles (DEP) have been shown to alter pulmonary immune responses to bacterial infection. Exposure of rats to 100 mg/m3 DEP for 4 hours was found to aggravate Listeria monocytogenes (Listeria) infection at 3 days post-infection, but the bacteria were largely cleared at 7 days post-infection due to the development of a strong T cell-mediated immunity. In the present study, we examined the effects of repeated DEP exposure at lower doses on pulmonary responses to bacterial infection. Brown Norway rats were exposed to DEP by inhalation at 20.62 ± 1.31 mg/m3, 4 hr/day for 5 days, followed by intratracheal inoculation with 100,000 Listeria at 2 hours after the last DEP exposure. DEP-exposed rats showed a significant increase in lung bacterial load at both 3 and 7 days post-infection. The repeated DEP exposure was shown to suppress both the innate, orchestrated by alveolar macrophages (AM), and T-cell mediated responses to Listeria. DEP inhibited AM production of interleukin (IL)-1{beta}, tumor necrosis factor-{alpha}, and IL-12, but enhanced Listeria-induced AM production of IL-10, which has been shown to prolong the survival of intracellular pathogens such as Listeria. DEP exposure also suppressed the development of bacteria-specific lymphocytes from lung-draining lymph nodes, as indicated by the decreased numbers of T lymphocytes and their CD4+ and CD8+ subsets. In addition, the DEP exposure markedly inhibited the Listeria-induced lymphocyte secretion of IL-2 at day 7, IL-10 at days 3 and 7, and interferon-{gamma} at days 3 to 10 post-infection when compared to air-exposed controls. These results show a sustained pattern of down-regulation of T-cell mediated immune responses by repeated low-dose DEP exposure, which is different from the results of a single high dose exposure, where the acute effect of DEP aggravated bacteria infection but triggered a strong T cell-mediated immunity.

Key Words: Diesel exhaust particles, inhalation, Listeria monocytogenes, alveolar macrophages, lymphocytes, cytokines .


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