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

L. Liu, H. Hu, H. Ji, A. D. Murdin, G. N. Pierce, G. Zhong

Research output: Contribution to journalArticle

50 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)123-128
Number of pages6
JournalMolecular and Cellular Biochemistry
Volume215
Issue number1-2
DOIs
StatePublished - Dec 1 2000

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Keywords

  • Chlamydial exacerbation of atherosclerosis

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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