(Circulation. 2001;103:2834.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
Chlamydia pneumoniae Infection Does Not Induce or Modify Atherosclerosis in Mice
From the Center for Molecular Medicine, Department of Medicine (G.C., G.K.H.), and the Microbiology and Tumor Biology Center (M.R., H.W.), Karolinska Institutet, Stockholm, Sweden; and INSERM, U430 (A.N.) and U460 (G.C.), Paris, France.
Correspondence to Göran K. Hansson, Center for Molecular Medicine L8:03, Karolinska Hospital, SE-17176 Stockholm, Sweden. E-mail goran.hansson{at}cmm.ki.se
Background—Seroepidemiological studies have linked Chlamydia pneumoniae (CP) to coronary heart disease, and recent experimental studies suggest that it may accelerate or even induce atherosclerosis. We therefore evaluated the effect of CP infection on atherosclerosis in atherosclerosis-prone apolipoprotein E–knockout (apoE-KO) and wild-type C57BL/6J mice.
Methods and Results—Six- to 8-week-old female mice were infected intranasally with live CP and then fed a standard chow diet for 22 weeks. A subgroup of mice was reinfected 18 weeks after primary infection. Polymerase chain reaction analysis of lung tissue confirmed successful infection with CP, and ELISA assays demonstrated development of a humoral immune response. Despite this, no statistically significant differences in aortic atherosclerotic lesions were found between CP-infected and control apoE-KO mice. Furthermore, CP infection did not induce atherosclerosis in C57BL/6J mice.
Conclusions—CP does not induce atherosclerosis in wild-type mice and does not accelerate atherosclerosis in chow-fed apoE-KO mice. Further studies will be necessary to clarify the explanation for the seroepidemiological association between CP and coronary heart disease in humans.
Key Words: atherosclerosis • hypercholesterolemia • infection
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