Ozone-Induced Modulation of Cell-Mediated Immune Responses in the Lungs

Most pulmonary immunotoxicology studies of ambient pollutants have been broadly designed to discern if overall humoral or cell-mediated immunity (CMI) was altered; few have assessed effects on particular aspects of immune function. We hypothesized that effects from ozone (O3) exposure on pulmonary C...

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Bibliographic Details
Published in:Toxicology and applied pharmacology 2001-03, Vol.171 (2), p.71-84
Main Authors: Cohen, Mitchell D., Sisco, Maureen, Li, Yun, Zelikoff, Judith T., Schlesinger, Richard B.
Format: Article
Language:English
Subjects:
Air
Animals
Biological and medical sciences
Cell Count
Colony Count, Microbial
Environmental pollutants toxicology
Hydrogen Peroxide - metabolism
Immunity, Cellular - drug effects
Immunity, Innate
Interferon-gamma - metabolism
Interleukin-1 - metabolism
Listeria monocytogenes - immunology
Listeriosis - immunology
Listeriosis - mortality
Lung - immunology
Lung - microbiology
Macrophages, Alveolar - immunology
Macrophages, Alveolar - metabolism
Male
Medical sciences
Neutrophils - immunology
Ozone - administration & dosage
Ozone - pharmacology
Rats
Rats, Inbred F344
Reactive Oxygen Species - metabolism
Superoxides - metabolism
Toxicology
Tumor Necrosis Factor-alpha - metabolism
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Summary:Most pulmonary immunotoxicology studies of ambient pollutants have been broadly designed to discern if overall humoral or cell-mediated immunity (CMI) was altered; few have assessed effects on particular aspects of immune function. We hypothesized that effects from ozone (O3) exposure on pulmonary CMI are linked in part to changes in local immune cell capacities to form and/or to interact with immunoregulatory cytokines. Rats exposed to 0.1 or 0.3 ppm O3 4 h/day 5 days/week, for 1 or 3 weeks were assessed for resistance to, and pulmonary clearance of, a subsequent Listeria monocytogenes challenge. In situ cytokine release and immune cell profiles were also analyzed at different stages of the antilisterial response. Although O3 exposure modulated CMI, effects were not consistently concentration- or duration-dependent. Exposure did not effect cumulative mortality from infection, but induced concentration-related effects upon morbidity onset and persistence. All 1-week exposed rats had listeric burdens trending higher than controls; 0.3 ppm rats displayed continual burden increases rather than any onset of resolution. Rats exposed for 3 weeks had no O3-related changes in clearance. No exposure-related effect on neutrophil or pulmonary macrophage (PAM) numbers or percentages was noted. Bacterial burden analyses with respect to cell type showed that Listeria:PAM ratios in 0.3 ppm rats ultimately became greatest compared to all other rats. In situ IL-1α and TNFα levels were consistently higher in O3-exposed rats. All rats displayed increasing in situ IFNγ levels as infection progressed, but no constant relationship was evident between IFNγ and initial IL-1α/TNFα levels in O3-exposed hosts. It seems that short-term (i.e., 1 week) repeated O3 exposures imparted more effects upon CMI than a more prolonged (i.e., 3 week) regimen, with effects manifesting at the level of the PAM and in the cytokine network responsible for immunoactivation.
ISSN:0041-008X
1096-0333
DOI:10.1006/taap.2000.9106