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Alveolar macrophage interaction with air pollution particulates
C A Goldsmith1, C Frevert, A Imrich
1Dept. of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA.
Environmental Health Perspectives
|December 24, 1997
Summary
Air pollution particles like ROFA and CAP increase light scatter in alveolar macrophages (AM), indicating uptake. Scavenger receptors mediate this uptake, and both particle types induce intracellular oxidant stress in AM.
Area of Science:
- Environmental toxicology
- Cellular immunology
- Respiratory medicine
Background:
- Alveolar macrophages (AM) are crucial in lung defense against inhaled pollutants.
- Air pollution particulates, including residual oil fly ash (ROFA) and concentrated ambient air particulates (CAP), pose a significant health risk.
- Understanding AM response to these particulates is vital for assessing their toxicological impact.
Purpose of the Study:
- To characterize the in vitro response of hamster AM to ROFA and CAP using flow cytometry.
- To investigate the role of scavenger-type receptors (SR) in the uptake of these particulates by AM.
- To quantify the intracellular oxidant stress induced by ROFA and CAP in AM.
Main Methods:
- Flow cytometric analysis of AM incubated with varying concentrations of ROFA or CAP.
- Measurement of AM-associated right angle light scatter (RAS) as an indicator of particle uptake.
- Assessment of intracellular oxidant stress using dichlorofluorescin oxidation.
- Inhibition studies using polyinosinic acid, a specific SR inhibitor.
Main Results:
- A dose-dependent increase in RAS was observed following AM uptake of both ROFA and CAP.
- Pretreatment with polyinosinic acid significantly inhibited the RAS increase, confirming the role of SR in particle uptake.
- Both ROFA and CAP induced a dose-related intracellular oxidant stress in AM, comparable to phorbol myristate acetate (PMA).
Conclusions:
- Flow cytometry of RAS increases is a valuable method for quantifying AM uptake of complex particulates.
- ROFA and CAP induce significant intracellular oxidant stress in AM, potentially contributing to inflammation.
- These findings highlight the cellular mechanisms underlying the respiratory toxicity of air pollution.