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Chlamydophila pneumoniae infection induces alterations in vascular contractile responses

Justin F Deniset1, Thomas E Hedley1, Elena Dibrov1

  • 1Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Department of Physiology, Faculties of Medicine and Pharmacy, University of Manitoba, Winnipeg, Manitoba, Canada.

The American Journal of Pathology
|January 5, 2012
PubMed

Insights

Chlamydophila pneumoniae infection directly impairs coronary artery contraction and relaxation. This study reveals how the bacterium alters vascular function, contributing to cardiovascular disease progression.

Area of Science:

  • Cardiovascular Research
  • Infectious Disease Immunology
  • Vascular Biology

Background:

  • Chlamydophila pneumoniae infection is linked to coronary artery disease.
  • The bacterium has been found in atherosclerotic plaques and can remodel vessel walls.
  • Direct effects of infection on arterial contractility are unknown.

Purpose of the Study:

  • To investigate the direct impact of C. pneumoniae infection on porcine coronary artery contractile function.
  • To elucidate the molecular mechanisms underlying infection-induced vascular alterations.

Main Methods:

  • Porcine left anterior descending coronary arteries were cultured and infected with C. pneumoniae.
  • Contractile responses to KCl and U46619, and relaxation to bradykinin and SNP were measured.
  • Expression levels of L-type Ca(2+) channels, IP3R, eNOS, and p22phox were assessed.

Main Results:

  • C. pneumoniae infection reduced KCl- and U46619-induced contractions.
  • Down-regulation of L-type Ca(2+) channels and IP3R levels was observed.
  • Endothelial-dependent relaxation was attenuated, with decreased eNOS expression and increased superoxide production.

Conclusions:

  • C. pneumoniae infection directly alters vascular contractile responses in coronary arteries.
  • The findings provide evidence for C. pneumoniae's role in cardiovascular disease pathogenesis.
  • Mechanisms involve altered calcium handling, impaired endothelial function, and oxidative stress.

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