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Chlamydia pneumoniae does not increase atherosclerosis in the aortic root of apolipoprotein E-deficient mice
K Aalto-Setälä1, K Laitinen, L Erkkilä
1Department of Internal Medicine, Tampere University Hospital, Finland. lokaaa@uta.fi
Insights
Chlamydia pneumoniae infection did not accelerate atherosclerosis in apolipoprotein E-deficient mice, regardless of diet. The bacteria were not detected in lesions, suggesting no causal link in this model.
Area of Science:
- Cardiovascular Research
- Infectious Disease Epidemiology
- Animal Models of Atherosclerosis
Background:
- Epidemiological studies suggest a link between cardiovascular disease and Chlamydia pneumoniae infection.
- Chlamydia pneumoniae has been found in atherosclerotic lesions, but a causal relationship remains unproven.
Purpose of the Study:
- To investigate the potential causal role of Chlamydia pneumoniae infection in the development of atherosclerosis.
- To determine if Chlamydia pneumoniae infection exacerbates atherogenic changes in apolipoprotein E-deficient mice.
Main Methods:
- Two strains of apolipoprotein E-deficient mice (FVB and C57BL/6J) were used.
- Mice were subjected to low- or high-fat diets and infected with Chlamydia pneumoniae multiple times.
- Atherosclerotic lesion size in the aortic root was measured, and bacterial presence in lesions was assessed via PCR.
Main Results:
- Chlamydia pneumoniae infection did not significantly alter the extent of atherosclerosis in either mouse strain or diet group.
- A high-fat diet increased atherosclerosis, and differences in susceptibility were noted between mouse strains.
- Chlamydia pneumoniae was not detected in atherosclerotic lesions, and no significant changes in serum lipid levels or myocardial inflammation were observed post-infection.
Conclusions:
- Under the experimental conditions, Chlamydia pneumoniae infection does not accelerate atherogenic changes in the aortic root of apoE-deficient mice.
- The findings do not support a direct causal role for Chlamydia pneumoniae in promoting atherosclerosis in this mouse model.
Abstract:
In epidemiological studies, an association between cardiovascular disease and Chlamydia pneumoniae (C pneumoniae) infection has been observed. Although C pneumoniae has been shown to be present in atherosclerotic lesions, a causal relationship between C pneumoniae infection and atherosclerosis has not been demonstrated. To study this question, we used 2 strains of apolipoprotein (apo) E-deficient mice. Eight-week-old mice on an FVB background that were maintained on either a low- or a high-fat diet were infected 3 times at 1-week intervals with C pneumoniae, and atherosclerotic lesions were measured in the aortic root at 10 weeks after the primary infection. In each of the diet groups, no difference in the extent of atherosclerosis could be observed between the C pneumoniae-infected and control animals. In further studies, 2 strains of apoE-deficient mice (FVB or C57BL/6J background) were infected 4 times at 3- to 4-week intervals, and the extent of atherosclerosis was analyzed 18 weeks later. The mice were kept on either a low- or a high-fat diet. The high-fat diet increased atherosclerosis, and a difference in atherosclerosis susceptibility between the mouse strains was observed. However, C pneumoniae infection did not influence lesion size in either mouse strain. On the other hand, C pneumoniae could not be demonstrated by polymerase chain reaction in any of the atherosclerotic lesions of the infected animals studied. A small decrease in serum cholesterol and triglyceride levels 3 days after the primary infection occurred, but after that no differences in serum lipid levels compared with those in noninfected animals were evident. In the myocardium of C pneumoniae-infected mice, no inflammatory signs could be observed. We conclude that under the experimental conditions used, C pneumoniae infection does not accelerate atherogenic changes in the aortic root of apoE-deficient mice.