Sensitivity to ozone, diesel exhaust particles, and standardized ambient particulate matter in rats with a listeria monocytogenes-induced respiratory infection

P.A. Steerenberg, A.P. Verlaan, A. de Klerk, A.J.F. Boere, H. van Loveren, F.R. Cassee

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Abstract

Sensitivity to ozone, diesel exhaust particles, and standardized ambient particulate matter in rats with a listeria monocytogenes-induced respiratory infection.

Steerenberg P, Verlaan A, De Klerk A, Boere A, Loveren H, Cassee F.

Laboratory for Toxicology, Pathology, and Genetics, National Institute of Public Health and the Environment, Bilthoven, The Netherlands. p.steerenberg@rivm.nl

Ambient particulate matter may increase respiratory allergic skewing of the T-cell-mediated immune response toward a T-helper-2 (Th2) response, with the consequence that the Th1 response develops less well. Successful clearing of a respiratory bacterial infection depends on an adequate Th1 immune response; therefore, the subject would not control the infection as well if exposed to particulate matter. To substantiate this hypothesis, we examined the effect of exposure to diesel exhaust particles (DEP) and urban particulate matter (EHC-93, Ottawa dust) on rats with a Listeria monocytogenes respiratory infection. Since this hypothesis has been confirmed for ozone, we used it as a positive control. Wistar rats were exposed to ozone (2 mg/m3 for 24 h/day for 7 days) and to DEP or to EHC-93 (50 microg/rat intranasally daily for 7 consecutive days). Twenty-four hours after the last exposure, the rats were infected intratracheally with 1 x 10(6) L. monocytogenes bacteria. The number of L. monocytogenes was determined after 3, 4 and 5 days. Statistically significant increases of the number of L. monocytogenes in rats exposed to ozone were observed in the lungs and spleen at all three times. However, we found no significant differences in the numbers of bacteria that were found in rats exposed to DEP or EHC-93 compared to the saline-treated group at any of the three times. In conclusion, the results of this study do not support the hypothesis that exposure to DEP or EHC-93 reduces subsequent resistance to a respiratory infection in rats. Copyright Taylor & Francis Inc.
Original languageEnglish
Pages (from-to)311-317
Number of pages7
JournalInhalation Toxicology
Volume16
Issue number5
DOIs
Publication statusPublished - 1 Jan 2004

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