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MODULATION OF HUMAN ALVEOLAR MACROPHAGE PROPERTIES BY OZONE EXPOSURE IN VITRO
Citation:
Becker, S., M. Madden, S. Newman, R. Devlin, AND H. Koren. MODULATION OF HUMAN ALVEOLAR MACROPHAGE PROPERTIES BY OZONE EXPOSURE IN VITRO. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-91/266 (NTIS PB92113281).
Description:
We have investigated changes in human alveolar macrophage (HAM) function after exposure in vitro to ozone (O3) (0.1-1.0 ppm for 2-4 hours). he functions studied reflect concern that 03 is detrimental to host defense mechanisms in the broncho-alveolar spaces. xposure of HAM to caused a concentration-dependent increase in release of prostaglandin E2 (PGE2), an important modulator of inflammation, phago-cytosis, and oxidative burst. lthough phagocytosis of particulate immune complexes was decreased by O3, we found no change in the quantity of Fc receptors and complement receptors on the HAM surface. Superoxide (O2-) production in response to phorbol ester (PMA) was reduced after exposure of HAM to O3 while the basal O2 release in response to plastic adherence was not affected. rowth inhibition of the opportunistic yeast Cryptococcus neoformans by HAM was not affected by O3 exposure. he production of inflammatory mediators and immune modulators such as tumor necrosis factor-alpha (TNF), interleukin 1 (IL-1) and interleukin 6 (IL-6) were not induced by exposure to the pollutant. owever, compared to controls, O3 exposed HAM produced significantly lower levels of these cytokines when stimulated with bacterial lipopolysaccharide (LPS). wo dimensional gel electrophoretic analysis of proteins made by HAM following In vitro exposure to O3 identified 11 proteins whose rate of synthesis was significantly altered. hus, these studies show that exposure to O3 alters the functional competence of HAM.
