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RECORD NUMBER: 558 OF 850

Main Title Ozone-Enhanced Pulmonary Infection with 'Streptococcus zooepidemicus' in Mice: The Role of Alveolar Macrophage Function and Capsular Virulence Factors.
Author Gilmour, M. I. ; Park, P. ; Selgrade, M. K. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Immunotoxicology Branch. ;North Carolina Univ. at Chapel Hill. Center for Environmental Medicine and Lung Biology.
Publisher c1993
Year Published 1993
Report Number EPA/600/J-93/376;
Stock Number PB93-231868
Additional Subjects Ozone ; Respiratory tract infections ; Alveolar marophages ; Virulence ; Toxicity ; Microbial colony count ; Mice ; In vitro analysis ; Phagocytosis ; Graphs(Charts) ; Mortality ; In vivo analysis ; Reprints ; Streptococcus zooepidemicus
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NTIS  PB93-231868 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 9p
Abstract
Ozone exposure has been shown to increase the susceptibility of mice to pulmonary bacterial infection. The differences in susceptibility of two strains of mice (C3H/HeJ and C57Bl/6) to pulmonary challenge with Streptococcus zooepidemicus are reported, and an association between O3 exposure, reduced alveolar macrophage (AM) function, and increased mortality to infection is demonstrated. After a 3-h exposure to air or to 0.4 or 0.8 ppm O3, mice received an infection of bacteria by aerosol. Subsequent mortality observed over a 20-day period for any given exposure concentration was greater in the C3H/HeJ mice than in the C57Bl/6 mice. Phagocytosis assays identified the AM from O3-exposed lungs as having an impaired ability to engulf the bacteria. Baseline phagocytic activity in C3H/HeJ mice was lower than that in C57Bl/6 mice. Microbiologic assessment of the lungs at various times after infection revealed that the streptococci proliferated rapidly in the lungs of O3-exposed mice, grew more quickly upon isolation, and displayed a mucoid colony appearance indicative of increased encapsulation. In vitro assays confirmed that the encapsulated isolates prevented binding of the bacteria to AM, and reinfection of nonexposed mice with the encapsulated isolate resulted in increased mortality compared with infection with similar numbers of the original unencapsulated bacteria.