DECREASED CD11B EXPRESSION, PHAGOCYTOSIS, AND OXIDATIVE BURST IN URBAN PARTICULATE POLLUTION-EXPOSED HUMAN MONOCYTES AND ALVEOLAR MACROPHAGES

Elevated levels of air pollution particulates less than or equal to 10 mu m in diameter (PM10) have been associated with an increase in mort ality and morbidity due to pulmonary complications, including pneumoni a. Impairment of inflammatory and host defense functions of the alveol ar macrophage (AM) may be a precipitating factor. The present study wa s undertaken to determine whether human AM and blood derived monocytes (MO) modulate the expression of receptors important for phagocytosis of opsonized microbes (cD11b, CD11c), gram-negative bacteria (CD14), e xtracellular matrix interaction (CD29), and immune responses (CD11a, C D54, HLA-DR) when exposed to particulates obtained from urban air (UAP ). Furthermore, phagocytosis of and oxidant generation by opsonized ye ast were investigated in particle-exposed cells. AM and MO exposed to UAP for 18 h expressed significantly lower levels of CD I Ib and CD29. CD14 expression was markedly decreased in MO but not in AM, and CD I Ic was reduced in AM but not in MO. CD I la, CD54, and HLA-DR were una ltered in both phagocyte populations. Decreased receptor expression wa s not dependent on particle load in the cells. Phagocytosis of Sacchar omyces cerevisiae and the chemiluminescence response were also signifi cantly inhibited by UAP. Time-course studies revealed that decreased o xidant generation was evident already at 3 h postexposure, while signi ficant effects on phagocytosis and CD11b expression were found at 18 h . These data indicate that exposure to particulate pollution is likely to impair host defense functions of AM and MO, which are important in elimination of a variety of pathogens in the lung.