Sensitivity to Ozone, Diesel Exhaust Particles, and Standardized Ambient Particulate Matter in Rats with aListeria Monocytogenes-Induced Respiratory Infection

Abstract

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.

Non-cancer health effects of diesel exhaust: A critical assessment of recent human and animal toxicological literature

“…In contrast to the findings discussed above, Steerenberg et al (2004) found that intranasal administration of DEP and EHC-93 (urban particulate matter collected in Ottawa, Canada) had no effect on the ability of rats to clear L. monocytogenes infection up to 5 days post-infection in both the lungs and the spleen, indicating that the immune system was not altered by the particulate exposure. Interestingly, ozone was used as a positive control in their study, and as expected, exposure to ozone (1 ppm) significantly impaired clearance of the bacteria from the rat lungs and spleen.…”

“…These results suggest that although high doses of DEP affected the immunological response to infection, the animals were still able to effectively counter the infections. Several studies found dose-dependent effects on susceptibility to infection extending to much lower DEP concentrations (30 µg/m 3 ), but Steerenberg et al (2004) notably found no significant effects of DEP exposure on clearance of L. monocytogenes infection with lower DEP exposure levels. Overall, the implications of the observed immunological effects in animals for human exposures are not entirely clear.…”

Eugenol attenuates pulmonary damage induced by diesel exhaust particles

“…Additionally, PAH and quinone play a key role in the activation of SAPKs, which regulate the expression of proinflammatory genes in macrophages (12), thus suggesting that oxidative stress is one of the mechanisms by which DEPs exert their toxic effects in the lungs. DEPs may, independently or in association with other material, present many diverse effects, including the decrease in alveolar macrophage function (35), impairment of mucociliary clearance, modification of the surfactant composition (10) and secretion (19), among other deleterious effects. Laks and coworkers (13) reported that metals and sulfur components of diesel affected particle toxicity to a lesser extent than its organic compounds.…”

The impact of surfactant protein-A on ozone-induced changes in the mouse bronchoalveolar lavage proteome

“…Approximately half of the DEF group of defense and immunity proteins underwent significant changes, with changes that included roughly equal numbers of increases and decreases. This "mixed" response may explain why ozone exposure has been reported to prime pulmonary innate immunity, and thereby enhance the response to LPS [111], while impairing clearance of pathogens that are dependent upon removal by cell-mediated immune mechanisms, including Listeria monocytogenes or Klebsiella pneumoniae [9,112]. There is precedent for selective changes in susceptibility.…”