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Iron enhances endothelial cell activation in response to Cytomegalovirus or Chlamydia pneumoniae infection

A E R Kartikasari1, N A Georgiou, M de Geest

  • 1University Medical Center Utrecht, Utrecht, the Netherlands.

European Journal of Clinical Investigation
|September 14, 2006
PubMed

Insights

Iron influences chronic infections like Chlamydia pneumoniae and cytomegalovirus, increasing endothelial activation and potentially contributing to atherosclerosis. Managing iron levels may be key in preventing this inflammatory disease.

Area of Science:

  • Cardiovascular Research
  • Infectious Diseases
  • Cell Biology

Background:

  • Chronic inflammation is implicated in atherosclerosis pathogenesis.
  • Pathogens like Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) can trigger endothelial activation, initiating the inflammatory cascade.
  • Iron's role in infection processes may exacerbate infection-mediated endothelial activation.

Purpose of the Study:

  • To investigate the impact of iron on endothelial activation induced by Cp and CMV infections.
  • To determine if iron modulates endothelial expression of adhesion molecules (ICAM-1, VCAM-1, E-selectin) in response to these pathogens.
  • To explore the mechanisms underlying iron's effect on infection-induced endothelial activation.

Main Methods:

  • Endothelial activation assessed via flow cytometry measuring ICAM-1, VCAM-1, and E-selectin expression.
  • Cytotoxicity evaluated using the MTT assay.
  • Cp and CMV infectivity quantified by immunostaining.

Main Results:

  • Increased endothelial cell infection correlated with higher adhesion molecule expression, suggesting paracrine signaling.
  • Iron additively upregulated Cp-induced VCAM-1 and synergistically potentiated Cp-induced ICAM-1 expression.
  • Iron enhanced ICAM-1 and VCAM-1 expression in conjunction with CMV, without altering initial infectivity. Iron's effects were reversible via chelation or radical scavenging.

Conclusions:

  • Endothelial response to chronic infections is dependent on intracellular iron levels.
  • Iron status in Cp or CMV-infected individuals may be a critical factor in atherosclerosis development.
  • Targeting iron levels could be a therapeutic strategy for preventing or mitigating atherosclerosis in infected populations.
Abstract

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