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Chlamydia pneumoniae accelerates coronary artery disease progression in transgenic hyperlipidemia-genetic

Victoria L M Herrera1, Li Shen, Lyle V Lopez

  • 1Section of Molecular Medicine and Molecular Genetics, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA. vherrera@bu.edu

Molecular Medicine (Cambridge, Mass.)
|October 23, 2003
PubMed

Insights

Chlamydia pneumoniae (Cpn) infection accelerates coronary artery disease (CAD) progression and reduces survival in a rat model, particularly in hyperlipidemic and hypertensive subjects. This suggests Cpn is a causal risk factor for CAD, driven by enhanced macrophage foam cell formation.

Area of Science:

  • Cardiovascular Research
  • Infectious Disease Immunology
  • Atherosclerosis Pathogenesis

Background:

  • Chlamydia pneumoniae (Cpn) is linked to human coronary artery disease (CAD), but its causal role remains unproven.
  • Existing animal models show Cpn exacerbates aortic atherosclerosis, yet its impact on CAD and survival is less understood.

Purpose of the Study:

  • To investigate the causal relevance of Cpn infection in the progression of coronary artery disease and its effect on survival.
  • To analyze Cpn's impact on macrophage foam cell formation in hyperlipidemic and hypertensive conditions.

Main Methods:

  • Utilized specific pathogen-free, inbred, transgenic-CAD Dahl salt-sensitive (S) hypertensive (Tg53) rats and control non-transgenic (nonTg) rats.
  • Inoculated rats with Cpn and assessed macrophage foam cell formation, CAD progression, and survival rates.
  • Analyzed transcription profiles of Cpn-infected macrophages versus controls.

Main Results:

  • Cpn infection accelerated macrophage foam cell formation in hyperlipidemic Tg53 rats, an effect dependent on hyperlipidemia.
  • Significant differences in transcription profiles were observed in Cpn-infected Tg53 macrophages.
  • Cpn-infected Tg53 rats exhibited decreased survival, linked to coronary plaques and atrial thrombi.

Conclusions:

  • Cpn infection, in the context of hyperlipidemia and hypertension, accelerates CAD progression in the Tg53 rat model.
  • The findings support Cpn as a causal risk factor for CAD progression.
  • Accelerated macrophage foam cell formation is a likely mechanism mediating Cpn's detrimental effects on CAD.

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