Alveolar Macrophage Interaction With Air Pollution Particulates

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Alveolar Macrophage Interaction With Air Pollution Particulates

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Title: Alveolar Macrophage Interaction With Air Pollution Particulates
Author: Goldsmith, C A; Frevert, C; Imrich, A; Sioutas, C; Kobzik, Lester

Note: Order does not necessarily reflect citation order of authors.

Citation: Goldsmith, C. A., C. Frevert, A. Imrich, C. Sioutas, and L. Kobzik. 1997. Alveolar macrophage interaction with air pollution particulates. Environmental Health Perspectives 105(Suppl 5): 1191-1195.
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Abstract: We applied flow cytometric analysis to characterize the in vitro response of alveolar macrophages (AM) to air pollution particulates. Normal hamster AM were incubated with varying concentrations of residual oil fly ash (ROFA) or concentrated ambient air particulates (CAP). We found a dose-dependent increase in AM-associated right angle light scatter (RAS) after uptake of ROFA (e.g., mean channel number 149.4 ± 6.5, 102.5 ± 4.1, 75.8 ± 3.5, and 61.0 ± 4.6 at 200, 100, 50, and 25 mg/ml, respectively) or CAP. A role for scavenger-type receptors (SR) in AM uptake of components of ROFA and CAP was identified by marked inhibition of RAS increases in AM pretreated with the specific SR inhibitor polyinosinic acid. We combined measurement of particle uptake (RAS) with flow cytometric analysis of intracellular oxidation of dichlorofluorescin. Both ROFA and CAP caused a dose-related intracellular oxidant stress within AM, comparable to that seen with phorbol myristate acetate (PMA) (e.g., fold increase over control, 6.6 ± 0.4, 3.6 ± 0.4, 4.6 ± 0.5, 200 mg/ml ROFA, 100 mg/ml ROFA, and \(10^{-7}\) M PMA, respectively). We conclude that flow cytometry of RAS increases provides a useful relative measurement of AM uptake of complex particulates within ROFA and CAP. Both ROFA and CAP cause substantial intracellular oxidant stress within AM, which may contribute to subsequent cell activation and production of proinflammatory mediators.
Published Version: doi:10.2307/3433531
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