Chlamydia pneumoniae infection significantly exacerbates aortic atherosclerosis in an LDLR-/- mouse model within six months

We have previously shown that infection with the C. pneumoniae AR39 strain once monthly for 9 consecutive months significantly exacerbated atheroscler osis in mice with LDL receptor deficiency (LDLR-/-) in the presence of a hi gh cholesterol diet. To further optimize the LDLR-/- mouse model for studyi ng the mechanisms of C. pneumoniae atherogenesis, we have tested a differen t infection protocol with intranasal inoculation twice monthly for 6 consec utive months in the present study. We found that C. pneumoniae infection fo r 6 months was sufficient to produce a 130%, significantly greater exacerba tion of aortic atherosclerosis in LDLR-/- mice in the presence of a high ch olesterol diet. Mice receiving a high cholesterol diet alone displayed a le sion area index of 18.2 +/- 6.1 (S.D.) while mice treated with both the hig h cholesterol diet and C. pneumoniae infection had a lesion area index of 4 1.8 +/- 15.2 (S.D.). However, the chlamydial infection did not significantl y alter the mouse serum total cholesterol or the LDL levels induced by the high cholesterol diet. This study not only confirms our previous findings t hat C. pneumoniae infection can exacerbate aortic atherosclerosis lesion in the LDLR-/- mice, but also further optimizes the LDLR-/- mouse model for f uture mechanism studies.