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Main Title Comparison of the Pulmonary Defenses against Streptococcal Infection in Rats and Mice Following 03 Exposure: Differences in Disease Susceptability and Neutrophil Recruitment.
Author Gilmour, M. I. ; Selgrade., M. K. ;
CORP Author North Carolina Univ. at Chapel Hill. Center for Environmental Medicine and Lung Biology. ;Health Effects Research Lab., Research Triangle Park, NC. Immunotoxicology Branch.
Publisher c1993
Year Published 1993
Report Number EPA-R-817643; EPA/600/J-94/195;
Stock Number PB94-163748
Additional Subjects Streptococcal infections ; Air pollution effects(Animals) ; Disease susceptibility ; Neutrophils ; Ozone ; Lung ; Comparison ; Rats ; Mice ; Toxicity ; Immunity ; Species diversity ; Phagocytosis ; Alveolar macrophages ; Reprint ; Streptococcus zooepidemicus
Library Call Number Additional Info Location Last
NTIS  PB94-163748 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 10p
To investigate the mechanism of disease protection in rats, antibacterial defenses of two strains of mice and F344 rats were compared. O3 exposure (3 hr, 0.4 or 0.8 ppm) and infection with S. zooepidemicus resulted in a dose-dependent proliferation of bacteria in the lungs of mice and high mortality. Polymorphonuclear leukocytes (PMNs) were observed in severely affected individuals 2 or more days postinfection and did not alter the fatal infection. In contrast, microbial inactivation was only impaired in O3-exposed rat lungs during the first 48 hr after infection. In these animals PMNs could be isolated from bronchoalveolar lavage fluid between 6 and 48 hr postinfection with the peak response occurring at 24 hr. Pretreatment with anti-PMN serum eliminated the neutrophil influx and impaired further the bactericidal activity in ozone-exposed rats. The results suggest that inhaled streptococci are cleared normally from the mouse lung by AMs. Following exposure to O3, AM phagocytosis is reduced and the mice develop a fatal infection. Differences in antimicrobial defenses between various experimental species and humans need to be better understood in order to predict effects of air pollutants on susceptibility to infection in man.