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Effect of Ozone on Lysosomal Enzymes of Alveolar Macrophages Engaged in Phagocytosis and Killing of Inhaled Staphylococcus aureus

The role of lysosomal enzymes in the inactivation of inhaled bacteria by alveolar macrophages was studied in rats infected with aerosols of Staphylococcus aureus and then exposed for 5 hr to 2.5 ppm of ozone to determine whether pollutant-induced defects in phagocytic killing were associated with re...

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Bibliographic Details
Published in:The Journal of infectious diseases 1978-09, Vol.138 (3), p.299-311
Main Authors: Goldstein, Elliot, Bartlema, Hotse C., Ploeg, Mels van der, Duijn, Pieter van, Stap, Johannes G. M. M. van der, Lippert, William
Format: Article
Language:English
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Summary:The role of lysosomal enzymes in the inactivation of inhaled bacteria by alveolar macrophages was studied in rats infected with aerosols of Staphylococcus aureus and then exposed for 5 hr to 2.5 ppm of ozone to determine whether pollutant-induced defects in phagocytic killing were associated with reductions in enzyme activity. Rates of bacterial ingestion and the activities of cellular acid phosphatase and β-glucuronidase were measured simultaneously in in situ perfused right lungs by sequential staining of frozen sections for enzyme and bacteria. Quantitative measurements of enzyme activity within macrophages without ingested bacteria were made with a computer-controlled cytospectrophotometry system. Exposure to ozone resulted in diminished rates of bacterial clearance and ingestion, large increases in numbers of intra- and extracellular staphylococcal microcolonies, and an absence of enzyme activity for macrophages containing bacterial microcolonies. Enzyme activity was unimpaired in macrophages without ingested bacteria. These results, in which absence of enzyme activity occurred only in macrophages subjected to the dual insults of ozone exposure and ingested bacteria, prove a relationship between impairment in bactericidal capacity and cellular activities of lysosomal enzyme.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/138.3.299