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Am J Physiol Lung Cell Mol Physiol 261: L277-L282, 1991;
1040-0605/91 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 261, Issue 4 277-L282, Copyright © 1991 by American Physiological Society

ARTICLES

Ozone reduces murine alveolar and peritoneal macrophage phagocytosis: the role of prostanoids

B. J. Canning, R. R. Hmieleski, E. W. Spannhake and G. J. Jakab
Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205.

Continuous ozone exposure (0.5 ppm, 1-14 days) reduced the phagocytic activity of murine alveolar and peritoneal macrophages. The response of peritoneal macrophages to ozone was virtually indistinguishable from the response of alveolar macrophages. When added exogenously, prostaglandin E2 (PGE2) inhibited alveolar and peritoneal macrophage phagocytosis. To test the hypothesis that prostanoids mediated the effects of ozone on macrophages, PGE levels of bronchoalveolar lavage fluid (BALF) and the phagocytic activity of macrophages from ozone-exposed mice pretreated with cyclooxygenase inhibitors were measured. PGE levels in BALF were increased following ozone exposure, with high levels of PGE associated with large decreases in phagocytic activity. Pretreatment with indomethacin and d-naproxen completely inhibited ozone-induced increases in PGE recovered by BAL and the suppression of peritoneal macrophage phagocytic activity. The inactive enantiomer of naproxen, l-naproxen, was without effect. Indomethacin partially inhibited ozone-induced suppression of alveolar macrophage phagocytic activity. These observations suggest that prostanoids play a key role in the response to ozone.


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