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Inhalation of ozone produces a decrease in superoxide anion radical production in mouse alveolar macrophages
J E Ryer-Powder1, M A Amoruso, B Czerniecki
1Department of Environmental and Community Medicine, UMDNJ-Robert Wood Johnson Medical School/Rutgers University, Piscataway 08854-5635.
Abstract:
The potentiation of fatal bacterial pneumonia in mice by prior inhalation of ozone occurs at levels of this oxidant pollutant that are frequently present in ambient air. A likely mechanism for this effect is an ozone-induced inhibition in the ability of pulmonary alveolar macrophages (PAM) to produce superoxide anion radical (O2-) demonstrated in the present study. A 25% decrease in PAM O2- production, as measured by nitroblue tetrazolium reduction, occurred after exposure of Swiss-Webster mice to 0.11 ppm ozone for 3 h (p less than 0.05). After 1 ppm there was almost complete inhibition of O2- release. In contrast, the rat, which is highly resistant to the potentiation of bacterial infections by ozone, was less sensitive to inhibition of PAM O2- production, as measured by cytochrome c reduction (mouse IC50, 0.41 ppm; rat IC50, 3.0 ppm ozone for 3 h). The observed decrement in mouse PAM O2- production was not associated with any change in phagocytic ability, as measured by both latex bead ingestion and 51Cr-labeled sheep red blood cell ingestion. This decrease in O2- production in the presence of normal phagocytic activity is analogous to certain of the findings in the neutrophils of children with chronic granulomatous disease. A decrease in rat PAM membrane cytochrome b558 levels was observed after ozone exposure of 3 ppm for 3 h, preliminarily suggesting that the mechanism by which ozone interferes with PAM O2- production may be through interaction with this heme-containing electron carrier.
Insights
Ozone exposure impairs pulmonary alveolar macrophages (PAMs) in mice, reducing their ability to produce superoxide anion radical (O2-), which is crucial for fighting bacterial pneumonia. This impairment occurs at common air pollution levels.
Area of Science:
- Environmental Health
- Immunotoxicology
- Pulmonary Medicine
Background:
- Ozone is a common air pollutant that can exacerbate respiratory infections.
- Pulmonary alveolar macrophages (PAMs) are critical immune cells in the lungs responsible for clearing pathogens.
- Ozone's impact on PAM function and its role in potentiating bacterial pneumonia are not fully understood.
Purpose of the Study:
- To investigate the mechanism by which ozone exposure potentiates bacterial pneumonia.
- To determine the effect of ozone on the superoxide anion radical (O2-) production by PAMs.
- To compare ozone's effect on PAMs in mice and rats, correlating with their known resistance to ozone-induced potentiation of infection.
Main Methods:
- Mice and rats were exposed to varying concentrations of ozone for 3 hours.
- PAMs were isolated, and their O2- production was measured using nitroblue tetrazolium reduction (mice) and cytochrome c reduction (rats).
- Phagocytic activity of PAMs was assessed using latex beads and sheep red blood cells. Cytochrome b558 levels were measured in rat PAMs.
Main Results:
- Ozone exposure significantly decreased O2- production in mouse PAMs, with near-complete inhibition at 1 ppm.
- Rats, which are more resistant to ozone's effects, showed less inhibition of PAM O2- production.
- Decreased O2- production in mice occurred without affecting phagocytic ability, and ozone exposure reduced cytochrome b558 levels in rat PAMs.
Conclusions:
- Ozone exposure inhibits the ability of mouse PAMs to produce O2-, a key mechanism for ozone-induced potentiation of bacterial pneumonia.
- Differences in ozone sensitivity between mice and rats correlate with their respective PAM O2- production inhibition.
- Ozone may interfere with PAM O2- production by interacting with membrane-bound electron carriers like cytochrome b558.