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Updated: Aug 8, 2026
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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
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, North Carolina 27599, United States.
Environmental Health Perspectives
|August 7, 2026
Summary
A new mouse model, CC002/Unc, shows increased sensitivity to ozone (O3) exposure compared to C57BL/6J mice. This strain offers a better model for studying ozone-induced lung disease mechanisms due to its human-like response.
Area of Science:
- Environmental Health
- 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 exhibit greater O3 sensitivity and less hypothermia than C57BL/6J mice.
Purpose of the Study:
- To evaluate CC002/Unc mice as a sensitive model for O3 exposure.
- To benchmark CC002/Unc against C57BL/6J mice.
- To identify genetic factors contributing to CC002/Unc's O3 sensitivity.
Main Methods:
- Mice (CC002/Unc and C57BL/6J) were exposed to acute or repeated O3.
- Quantitative trait loci (QTL) mapping was performed in a CC002/Unc x CC005/TauUnc backcross population.
- Respiratory and lung inflammation responses were analyzed.
Main Results:
- CC002/Unc mice showed significantly higher inflammation and injury after O3 exposure compared to C57BL/6J.
- CC002/Unc mice exhibited reduced breathing frequency and hypothermia.
- Five QTL for airway eosinophilia were identified, with a major QTL on chromosome 11.
Conclusions:
- CC002/Unc mice provide a more sensitive and human-like model for studying O3 effects.
- Genetic mapping identified key regions associated with O3-induced airway inflammation.
- Further research on CC002/Unc susceptibility genes can elucidate O3-induced lung disease mechanisms.
