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FACTORS THAT INFLUENCE THE SUPPRESSION OF PULMONARY ANTIBACTERIAL DEFENSES IN MICE EXPOSED TO OZONE
Citation:
Gilmour, M.I., P. Park, D. Doerfler, AND M. Selgrade. FACTORS THAT INFLUENCE THE SUPPRESSION OF PULMONARY ANTIBACTERIAL DEFENSES IN MICE EXPOSED TO OZONE. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-93/398 (NTIS PB93236354), 1993.
Description:
Exposure to ozone (03) has been shown to increase susceptibility of mice to bacterial infection; however the underlying mechanism has not been well elucidated. his study investigated the effect Of 03 exposure on the ability of mice to combat an infectious challenge of Streptococcus zooepidemicus. ollowing a 3hr exposure to either air, 0.4, or 0.8 ppm O3, 5 and 9 week old mice received an aerosol infection of bacteria. ntrapulmonary killing of the bacteria was impaired in the O3-exposed mice. he effect was most severe at the higher dose of O3 in the younger mice, and showed good correlation to subsequent mortality assessed over a 20 day period. lveolar macrophages (AM) from O3 exposed mice had an impaired ability to phagocytose the bacteria. dditionally, prostaglandin E2 (PGE2) levels which are known to depress AM function, were increased in the bronchoalveolar lavage fluid of the younger mice following exposure to O3, while pretreatment with indomethacin in the drinking water blunted the increased production of PGE2, and reduced O3 enhanced mortality from 60% to 47%. he data show that 03 inhalation can reduce the defensive capability of the murine lung, and that this is associated with a reduction in AM phagocytosis. he defect is more marked in young mice, suggesting that they may be more susceptible to oxidant exposure. urther studies are required to distinguish between direct toxicity of O3 on the AM, and indirect suppression due to pharmacologic or inflammatory meditors.