Effects of Inhaled Ozone on Pulmonary Immune Cells Critical to Antibacterial Responses in Situ

Abstract

The goal of this study was to examine effects from repeated exposure to ozone (O 3 ) on immune cells involved in cell-mediated antibacterial responses in the lungs. Rats exposed to 0.1 or 0.3 ppm O 3 for 4 h/ day, 5 days/ wk, for 1 or 3 wk were analyzed for the ability to clear an intrapulmonary challenge with Listeria monocytogenes or had their lungs processed to obtain pulmonary alveolar macrophages (PAM) and lung-associated lymphocytes for analyses of select cell functions and surface marker expression. The results indicate that repeated inhalation exposure to O 3 affected local cell-mediated immunity ( CMI) responses as evidenced by effects on clearance of Listeria. However, this modulation was not consistently dependent on exposure concentration or duration. Short-term repeat exposures had more effect on host resistance than did the more prolonged regimen, with rats exposed to 0.1 ppm O 3 most adversely impacted. Clearance patterns suggest modifications in innate resistance following 1 wk of exposure to 0.1 ppm O 3 , but no similar effect following a 3-wk regimen. Exposure to 0.3 ppm O 3 appeared to affect both innate and acquired resistance after a 1-wk regimen, but mainly the former after an additional 2 wk of exposure. We conclude that these two mechanisms of resistance are differentially affected by O 3 and that distinct time-and O 3 concentration-dependent adaptation phenomena evolve for each; that is, in situ adaptation to higher levels of O 3 may occur more readily with acquired than with innate/ PAM-dependent resistance. A similar pattern of inconsistent effect on PAM and lung-associated lymphocytes was also evident. For example, while 3-wk exposures had a greater effect on PAM reactive oxygen intermediate ROI production, evidence 599

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

“…One may presume that the lung tissue, including macrophages, is damaged by ozone exposure, which results in an immediate effect on the host defense against L. monocytogenes. Indeed, phagocytic activity of macrophages in ozone-exposed rats was diminished (van Loveren et al, 1988;Cohen et al, 2002). However, van Loveren et al (1988) show that not only the innate immunity but also the T-cell-mediated immune responses are affected.…”

“…Subsequent exposures to other exogenous factors such as bacteria or viruses may therefore cause an increased inflammatory response. Indeed, studies show that rats exposed to ozone were less able to cope with the L. monocytogenes infection than were healthy controls (Cohen et al, 2001(Cohen et al, , 2002van Loveren et al, 1988).…”

“…Second, the bacteria concentration was ten times greater in our experiments, which might lead to the observed differences. Cohen et al (2002) show that a doubling of the Listeria concentration (8 × 10 6 vs. 4 × 10 6 CFU) could change the outcome after ozone exposure. Third, the Brown-Norway rat, used by Yin et al (2002), is a Th2 responder, while the Wistar rat, used in the present study, is a Th1 responder.…”

“…Exposure to ozone suppressed ovalbumin-induced IgG2a in sensitized mice (Neuhaus-Steinmetz et al, 2000), but exposure to EHC-93 in this animal model increased the levels of ovalbumin-specific IgE, IgG1, and IgG2a (Steerenberg et al, 2003a(Steerenberg et al, , 2003b. It has also been shown that ozone downregulates the IgG2a response in an animal model for respiratory infection (van Loveren et al, , 1988Steerenberg et al, 1996;Cohen et al, 2002). Yin et al (2002) find increased levels of Listeria monocytogenes after coexposure of Listeria bacteria and DEP in their respiratory infection model.…”

Immunotoxicology of arc welding fume: Worker and experimental animal studies

“…Interestingly, and in contrast to MMA-SS fume and soluble Cr, GMA-SS fume inhalation reduced ROS production from AM measured via chemiluminesence. Attenuated AM activity has also been found in conjunction with reduced bacterial clearance after diesel and O 3 exposure (van Loveren et al, 1988;Cohen et al, 2002;Yin et al, 2002). Inhalation exposure to GMA-MS fume (40 mg/m 3 × 3 h/day × 10 days) did not result in an overt lung inflammatory response, but significantly reduced pulmonary bacterial clearance.…”