Record Display for the EPA National Library Catalog

RECORD NUMBER: 16 OF 21

Main Title Ozone Effect on Respiratory Syncytial Virus Infectivity and Cytokine Production by Human Alveolar Macrophages.
Author Soukup, J. ; Koren, H. S. ; Becker., S. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Human Studies Div. ;TRC Environmental Corp., Chapel Hill, NC.
Publisher c1993
Year Published 1993
Report Number EPA/600/J-94/215;
Stock Number PB94-163946
Additional Subjects Respiratory syncytial virus ; Cytokines ; Ozone ; Air pollution effects(Humans) ; Toxicity ; Alveolar macrophages ; Virulence ; Tumor necrosis factor ; Interleukin-1 ; Interleukin-6 ; Biosynthesis ; Reprint ;
Holdings
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Status
NTIS  PB94-163946 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 11p
Abstract
The study was performed to evaluate the effect of ozone (O3) exposure at 1 ppm for 2 hr on the susceptibility/resistance of adult human alveolar macrophages (AM) to infection with respiratory syncytial virus (RSV) in vitro and on RSV-induced cytokine production by the AM. AM were first exposed to O3 or to filtered air and then infected with RSV at multiplicities of infection (m.o.i.) of 0.1 1.0 and 10. The percentage RSV-infected AM and the amount of infectious virus released by the cells were determined at Days 2 and 4 after infection. Interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF) levels in the supernatants were determined on Day 2. No difference in the percentage infected AM or in the amount of infectious RSV produced was found between control and O3-exposed cultures. However, O3-exposed AM infected with RSV at m.o.i. 1 produced less IL-1 in response to RSV infection than control AM:63.6 pg/ml compared with 98.5 pg/ml. No difference in IL-1 was seen with m.o.i. 10. IL-6 levels were also decreased, but only after infection with m.o.i. 0.1. At this level of infection 830 pg/ml was produced by control AM as compared to 468.2 pg/ml by O3-exposed AM. TNF production was unaffected by O3 at all multiplicities of infection. (Copyright (c) 1993 by Academic Press, Inc.)