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Chlamydia pneumoniae infection significantly exacerbates aortic atherosclerosis in an LDLR-/- mouse model within six
1Department of Medical Microbiology, St. Bonilace General Hospital Research Centre, University of Manitoba, Canada.
Insights
Chlamydia pneumoniae infection significantly worsens atherosclerosis in a mouse model. This study refines the model for future research into how C. pneumoniae causes this cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Infectious Disease Research
- Animal Models of Atherosclerosis
Background:
- Chlamydia pneumoniae infection is a suspected contributor to atherosclerosis.
- Previous studies showed C. pneumoniae exacerbates atherosclerosis in LDLR-/- mice.
- Optimization of the LDLR-/- mouse model is needed for mechanistic studies.
Purpose of the Study:
- To optimize the LDLR-/- mouse model for studying C. pneumoniae-induced atherogenesis.
- To evaluate a new intranasal infection protocol (twice monthly for 6 months).
- To confirm C. pneumoniae's role in exacerbating atherosclerosis.
Main Methods:
- Utilized LDL receptor-deficient (LDLR-/-) mice.
- Administered intranasal C. pneumoniae AR39 strain twice monthly for 6 months.
- Maintained mice on a high-cholesterol diet.
Main Results:
- C. pneumoniae infection significantly increased aortic atherosclerosis by 130% (lesion area index 41.8 vs 18.2).
- Infection did not significantly alter serum total cholesterol or LDL levels.
- The optimized protocol demonstrated a robust exacerbation of atherosclerosis.
Conclusions:
- A 6-month intranasal C. pneumoniae infection protocol effectively exacerbates atherosclerosis in LDLR-/- mice.
- This optimized model is suitable for investigating the mechanisms of C. pneumoniae-driven atherogenesis.
- C. pneumoniae infection exacerbates atherosclerosis independently of significant changes in host lipid levels.
Abstract:
We have previously shown that infection with the C. pneumoniae AR39 strain once monthly for 9 consecutive months significantly exacerbated atherosclerosis in mice with LDL receptor deficiency (LDLR-/-) in the presence of a high cholesterol diet. To further optimize the LDLR-/- mouse model for studying the mechanisms of C. pneumoniae atherogenesis, we have tested a different infection protocol with intranasal inoculation twice monthly for 6 consecutive months in the present study. We found that C. pneumoniae infection for 6 months was sufficient to produce a 130%, significantly greater exacerbation of aortic atherosclerosis in LDLR-/- mice in the presence of a high cholesterol diet. Mice receiving a high cholesterol diet alone displayed a lesion area index of 18.2 +/- 6.1 (S.D.) while mice treated with both the high cholesterol diet and C. pneumoniae infection had a lesion area index of 41.8 +/- 15.2 (S.D.). However, the chlamydial infection did not significantly alter the mouse serum total cholesterol or the LDL levels induced by the high cholesterol diet. This study not only confirms our previous findings that C. pneumoniae infection can exacerbate aortic atherosclerosis lesion in the LDLR-/- mice, but also further optimizes the LDLR-/- mouse model for future mechanism studies.