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Alveolar macrophage cytokine response to air pollution particles: oxidant mechanisms.

ABSTRACT: Alveolar macrophages (AMs) primed with LPS and treated with concentrated ambient air particles (CAPs) showed enhanced release of tumor necrosis factor (TNF) and provide an in vitro model for the amplified effects of air pollution particles seen in people with preexisting lung disease. To investigate the mechanism(s) by which CAPs mediate TNF release in primed rat AMs, we first tested the effect of a panel of antioxidants. N-Acetyl-l-cysteine (20 mM), dimethyl thiourea (20 mM) and catalase (5 microM) significantly inhibited TNF release by primed AMs incubated with CAPs. Conversely, when LPS-primed AMs were treated with CAPs in the presence of exogenous oxidants (H(2)O(2) generated by glucose oxidase, 10 microM/h), TNF release and cell toxicity was significantly increased. The soluble fraction of CAPs suspensions caused most of the increased bioactivity in the presence of exogenous H(2)O(2). The metal chelator deferoxamine (DFO) strongly inhibited the interaction of the soluble fraction with H(2)O(2) but had no effect on the bioactivity of the insoluble CAPs fraction. We conclude that CAPs can mediate their effects in primed AMs by acting on oxidant-sensitive cytokine release in at least two distinct ways. In the primed cell, insoluble components of PM mediate enhanced TNF production that is H(2)O(2)-dependent (catalase-sensitive) yet independent of iron (DFO-insensitive). In the presence of exogenous H(2)O(2) released by AMs, PMNs, or other lung cells within an inflamed alveolar milieu, soluble iron released from air particles can also mediate cytokine release and cell toxicity.

SUBMITTER: Imrich A

PROVIDER: S-EPMC1852536 | biostudies-literature | 2007 Feb

REPOSITORIES: biostudies-literature

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Alveolar macrophage cytokine response to air pollution particles: oxidant mechanisms.

Imrich Amy A Ning YaoYu Y Lawrence Joy J Coull Brent B Gitin Elena E Knutson Mitchell M Kobzik Lester L

Toxicology and applied pharmacology 20061215 3

Alveolar macrophages (AMs) primed with LPS and treated with concentrated ambient air particles (CAPs) showed enhanced release of tumor necrosis factor (TNF) and provide an in vitro model for the amplified effects of air pollution particles seen in people with preexisting lung disease. To investigate the mechanism(s) by which CAPs mediate TNF release in primed rat AMs, we first tested the effect of a panel of antioxidants. N-Acetyl-l-cysteine (20 mM), dimethyl thiourea (20 mM) and catalase (5 mic ...[more]

PMID: 17222881

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Project description:It is well known that exceeded levels of particulate matter in the air and other air pollutants harmfully affect the cardiovascular system. Empirical analyses of the effects of these factors on stroke incidence and mortality are still limited. The main objective of our analyses was to determine the association between short-term exposure to air pollutants and stroke incidence in non-industrial areas, more specifically in north-eastern Poland. To achieve this aim, we used data from the National Health Fund on patients hospitalized for stroke between 2011 and 2020 in the largest city of the region described as the Green Lungs of Poland. The pollution levels and atmospheric conditions data were obtained from the Provincial Inspectorate for Environmental Protection and the Institute of Meteorology and Water Management. Using daily data on hospitalizations, atmospheric conditions, and pollution, as well as ordered logistic regression models the hypotheses on the impact of weather and air pollution conditions on ischemic strokes were tested. The study group included 4838 patients, 45.6% of whom were male; the average patient age was approximately 74 years. The average concentrations of PM2.5 were 19.09 µg/m3, PM10 26.66 µg/m3 and CO 0.35 µg/m3. Analyses showed that an increase in PM2.5 and PM10 concentrations by 10 µg/m3 was associated with an increase in the incidence of stroke on the day of exposure (OR = 1.075, 95% CI 0.999-1.157, P = 0.053; OR = 1.056, 95% CI 1.004-1.110, P = 0.035) and the effect was even several times greater on the occurrence of a stroke event in general (PM2.5: OR = 1.120, 95% CI 1.013-1.237, P = 0.026; PM10: OR = 1.103, 95% CI 1.028-1.182, P = 0.006). Furthermore, a short-term (up to 3 days) effect of CO on stroke incidence was observed in the study area. An increase of 1 μg/m3 CO was associated with a lower incidence of stroke 2 days after the exposure (OR = 0.976, 95% CI 0.953-0.998, P = 0.037) and a higher incidence 3 days after the exposure (OR = 1.026, 95% CI 1.004-1.049, P = 0.022).

Dataset Information

Alveolar macrophage cytokine response to air pollution particles: oxidant mechanisms.

Publications

Alveolar macrophage cytokine response to air pollution particles: oxidant mechanisms.

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