Chlamydia pneumoniae does not increase atherosclerosis in the aortic root of apolipoprotein E-deficient mice

In epidemiological studies, an association between cardiovascular disease a nd Chlamydia pneumoniae (C pneumoniae) infection has been observed. Althoug h C pneumoniae has been shown to be present in atherosclerotic lesions, a c ausal relationship between C pneumoniae infection and atherosclerosis has n ot been demonstrated. To study this question, we used 2 strains of apolipop rotein (apo) E-deficient mice. Eight-week-old mice on an FVB background tha t 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 me asured 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) wer e infected 4 times at 3- to 4-week intervals, and the extent of atheroscler osis 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 differenc e in atherosclerosis susceptibility between the mouse strains was observed. However, C pneumoniae infection did not influence lesion size in either mo use strain. On the other hand, C pneumoniae could not be demonstrated by po lymerase chain reaction in any of the atherosclerotic lesions of the infect ed animals studied. A small decrease in serum cholesterol and triglyceride levels 3 days after the primary infection occurred, but after that no diffe rences in serum lipid levels compared with those in noninfected animals wer e evident. In the myocardium of C pneumoniae-infected mice, no inflammatory signs could be observed. We conclude that under the experimental condition s used, C pneumoniae infection does not accelerate atherogenic changes in t he aortic root of apoE-deficient mice.