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Updated: Jun 22, 2026
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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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A new mouse model for ozone health effects research
Gregory J Smith1, Robert M Immormino2, Martin T Ferris1
1Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Environmental Health Perspectives
|June 5, 2025
Summary
The CC002/Unc mouse strain shows greater sensitivity to ozone (O3) exposure than the standard C57BL/6J strain, offering a better model for studying respiratory health effects. This enhanced sensitivity is linked to a more human-like thermoregulatory response.
Area of Science:
- Environmental Health Sciences
- Toxicology
- Genetics
Background:
- Ozone (O3) exposure is linked to respiratory issues.
- Rodent models for O3 research have limitations due to species-specific hypothermia responses.
- CC002/Unc mice may offer a more sensitive and human-relevant model for O3 studies.
Purpose of the Study:
- To evaluate CC002/Unc mice as a sensitive model for ozone (O3) response compared to C57BL/6J mice.
- To identify genetic factors contributing to CC002/Unc's sensitivity to O3 exposure.
Main Methods:
- CC002/Unc and C57BL/6J mice were exposed to acute or repeated levels of O3.
- Quantitative trait loci (QTL) mapping was performed using a backcross population derived from CC002/Unc and an O3-resistant strain.
- Physiological responses, including breathing frequency and thermoregulation, were monitored.
Main Results:
- CC002/Unc mice exhibited significantly greater inflammation and lung injury following O3 exposure compared to C57BL/6J mice.
- Enhanced sensitivity in CC002/Unc mice was associated with reduced hypothermia.
- Repeated O3 exposure led to eosinophilic inflammation and fibrosis in CC002/Unc lungs.
- Five QTLs for airway eosinophilia were identified, with a major locus on chromosome 11.
Conclusions:
- The CC002/Unc strain serves as a superior model for studying O3-induced lung disease due to its heightened sensitivity and more human-like thermoregulation.
- Further genetic investigation of CC002/Unc susceptibility can elucidate mechanisms of O3 toxicity.
- This research provides a valuable platform for understanding human respiratory responses to ambient ozone.
