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Radiation-induced strain differences in mouse alveolar inflammatory cell apoptosis
Thomas J O'Brien1, Séverine Létuvé, Christina K Haston
1Meakins-Christie Laboratories, Department of Medicine, McGill University, Montreal, QC, Canada.
Canadian Journal of Physiology and Pharmacology
|March 11, 2005
Summary
Differences in lung inflammatory cell apoptosis may explain why C3H/HeJ (C3H) mice show a severe response to whole-thorax irradiation compared to C57BL/6J (B6) mice, with B6 mice exhibiting higher apoptosis rates.
Area of Science:
- Radiation biology
- Immunology
- Pulmonary medicine
Background:
- Whole-thorax irradiation induces varying degrees of lung inflammation and fibrosis in different mouse strains.
- C3H/HeJ (C3H) mice develop diffuse alveolitis, while C57BL/6J (B6) mice exhibit a milder response with fibrosis.
Purpose of the Study:
- To investigate if differences in lung inflammatory cell apoptosis contribute to the observed strain-dependent responses to thoracic radiation.
- To compare the rates of apoptosis in lung inflammatory cells between C3H and B6 mice after irradiation.
Main Methods:
- C3H and B6 mice received 18 Gy whole-thorax irradiation.
- Animals were sacrificed at 11 or 18 weeks post-irradiation or when moribund.
- Active caspase-3 staining was used to quantify apoptotic cells in lung histology.
Main Results:
- B6 mice showed a significantly higher apoptotic index (17.8%) compared to C3H mice (7.8%) at 11 weeks post-irradiation (p=0.028).
- In moribund mice, B6 mice also had a greater apoptotic index (27.3%) than C3H mice (14.4%) (p=0.036).
- No C3H mice survived to the 18-week time point.
Conclusions:
- A higher rate of inflammatory cell apoptosis, primarily alveolar macrophages, in B6 mice may contribute to their milder pulmonary radiation response.
- Differences in inflammatory cell apoptosis are a potential mechanism underlying strain-specific lung radiosensitivity.