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Iron mediates differential activation of human endothelial cells in response towards Chlamydia pneumoniae or Cytomegalovirus infection

Chronic inflammation has been implemented in the pathogenesis of inflammatory diseases like atherosclerosis. Several pathogens like Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) result in inflammation and thereby are potentially artherogenic. Those infections could trigger endothelial activation, the starting point of the atherogenic inflammatory cascade. Considering the role of iron in a wide-range of infection processes, the presence of iron may complicate infection-mediated endothelial activation. In this study, we measure endothelial ICAM-1, VCAM-1 and Eselection expression using flow cytometry, as an indication of endothelial activation.

An increased number of infected endothelial cells in a monolayer population lead to a raised expression of adhesion molecules of the whole cell population, suggesting paracrine interactions. Iron additively upregulated Cp-induced VCAM-1 expression, while synergistically potentiated Cp-induced ICAM-1 expression. Together with CMV, iron also stimulated ICAM-1 and VCAM-1 expression.

Moreover, the effects of iron could be reversed by intracellular iron chelation or radical scavenging, conforming modulating effects of iron on endothelial activation after infections through an increased cellular oxidative stress. We conclude that endothelial response towards chronic infections is alterable by intracellular iron levels.

Conclusion: This finding implies that iron status in populations positive for Cp or CMV infections could be an important determinant in having increased risk of developing atherosclerosis.

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