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Atherogenic effects of Chlamydia pneumoniae: refuting the innocent bystander hypothesis

Craig H Selzman1, Mihai G Netea, Michael A Zimmerman

  • 1Division of Cardiothoracic Surgery, University of North Carolina School of Medicine, Wing C, CB 7065, Chapel Hill, NC 27599, USA.

The Journal of Thoracic and Cardiovascular Surgery
|September 23, 2003
PubMed

Insights

Chlamydia pneumoniae infection significantly increases vascular smooth muscle cell proliferation and promotes atherogenic cytokine release, indicating its role in atherosclerosis development. Treatment with azithromycin abrogated these effects.

Area of Science:

  • Cardiovascular Research
  • Infectious Diseases
  • Cell Biology

Background:

  • Chlamydia pneumoniae infection is linked to atherosclerosis, but its direct role is debated.
  • Previous studies suggest C. pneumoniae presence in cardiovascular lesions, yet mechanistic links to atherogenesis are scarce.

Purpose of the Study:

  • To investigate the pathophysiologic role of C. pneumoniae in human vascular smooth muscle cells.
  • To determine the effect of C. pneumoniae infection on vascular smooth muscle cell proliferation, cell-cycle proteins, and cytokine release.

Main Methods:

  • Human aortic vascular smooth muscle cells were infected with C. pneumoniae in vitro.
  • Cell proliferation was measured using mitochondrial activity, cell counting, and PCNA staining.
  • p53 expression, IL-6, and IL-8 levels were analyzed.

Main Results:

  • C. pneumoniae infection led to a 2-3 fold increase in vascular smooth muscle cell proliferation.
  • Infection increased proliferating cell nuclear antigen (PCNA) expression and decreased p53 binding.
  • Released levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) increased by 2.5-fold.

Conclusions:

  • C. pneumoniae infection stimulates vascular smooth muscle cell proliferation and the release of atherogenic cytokines.
  • The findings suggest C. pneumoniae actively participates in atherogenesis, not merely as an bystander.
  • Azithromycin effectively counteracted the effects of C. pneumoniae infection in vitro.
Abstract

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