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Azithromycin reduces Chlamydia pneumoniae-induced attenuation of eNOS and cGMP production by endothelial cells

J J M Bouwman1, F L J Visseren, L M Bevers

  • 1Department of Medical Microbiology and Immunology, Diakonessen Hospital Utrecht, Utrecht, The Netherlands. jbouwman@diakhuis.nl

European Journal of Clinical Investigation
|September 1, 2005
PubMed
Abstract

Insights

Chlamydia pneumoniae infection reduces endothelial nitric oxide synthase (eNOS) and cyclic guanosine monophosphate (cGMP) production. Azithromycin treatment reversed these effects, suggesting its potential in treating infection-induced atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Infectious Diseases
  • Endothelial Biology

Background:

  • Atherosclerosis may be linked to intracellular infections like cytomegalovirus (CMV) and Chlamydia pneumoniae (Cp).
  • Endothelial nitric oxide synthase (eNOS) dysfunction, leading to reduced nitric oxide (NO) and increased reactive oxygen species (ROS), is implicated in atherosclerosis.
  • This study investigated the impact of Cp and CMV infections on NO metabolism and the potential of azithromycin to reverse these changes.

Purpose of the Study:

  • To investigate the effect of Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) infection on endothelial nitric oxide synthase (eNOS), cyclic guanosine monophosphate (cGMP), and reactive oxygen species (ROS) production in human umbilical vein endothelial cells (HUVECs).
  • To determine if azithromycin treatment can reverse infection-induced alterations in endothelial function.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were infected with Cp or CMV.
  • Production of eNOS, cGMP, and ROS was measured post-infection.
  • Infected HUVECs were treated with varying concentrations of azithromycin to assess its reversing effects.

Main Results:

  • Cp and CMV infections significantly reduced eNOS production in HUVECs.
  • Cp infection, but not CMV, decreased cGMP production.
  • Cp infection led to a dose-dependent reduction in ROS production.
  • Azithromycin treatment dose-dependently restored eNOS, cGMP, and ROS production in Cp-infected HUVECs.

Conclusions:

  • In vitro, Cp infection impairs endothelial cell function by reducing eNOS, cGMP, and ROS production.
  • Azithromycin effectively reverses the detrimental effects of Cp infection on endothelial cells.
  • These findings support the use of antibiotic therapy, specifically azithromycin, for improving endothelial function in infection-induced atherosclerosis.

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