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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
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Androgens augment pulmonary responses to ozone in mice
Ross S Osgood1, David I Kasahara1, Hiroki Tashiro1
1Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Physiological Reports
|September 24, 2019
Summary
Androgens worsen ozone-induced airway hyperresponsiveness in male mice. Castration or androgen receptor blockers reduced this effect, suggesting androgens play a key role in ozone
Area of Science:
- Environmental toxicology
- Pulmonary immunology
- Endocrinology
Background:
- Ozone exposure is a significant asthma trigger, causing airway hyperresponsiveness.
- Male mice exhibit greater ozone-induced airway hyperresponsiveness than females, implying sex hormone involvement.
Purpose of the Study:
- To investigate the role of androgens in sex-based differences in ozone-induced airway hyperresponsiveness.
- To determine if androgen receptor blockade affects pulmonary responses to ozone.
Main Methods:
- Castration or sham surgery in mice at 4 weeks of age.
- Ozone exposure (2 ppm, 3 hours) at 8 weeks, followed by methacholine challenge.
- Analysis of airway hyperresponsiveness and bronchoalveolar lavage cell counts and cytokine levels.
Main Results:
- Castration significantly attenuated ozone-induced airway hyperresponsiveness and reduced bronchoalveolar lavage cells.
- Androgen receptor inhibition with flutamide mimicked the effects of castration.
- Interleukin-1 alpha (IL-1α) levels were reduced by castration and flutamide, but anti-IL-1α treatment did not alter airway hyperresponsiveness.
Conclusions:
- Androgens augment pulmonary responses to ozone, contributing to airway hyperresponsiveness.
- IL-1α may mediate androgen effects on ozone-induced lung inflammation but not hyperresponsiveness.
