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Iron enhances endothelial cell activation in response to Cytomegalovirus or Chlamydia pneumoniae infection
Author(s) -
Kartikasari A. E. R.,
Georgiou N. A.,
De Geest M.,
Van KatsRenaud J. H.,
Bouwman J. J. M.,
Van Asbeck B. S.,
Marx J. J. M.,
Visseren F. L. J.
Publication year - 2006
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2006.01709.x
Subject(s) - endothelial activation , population , endothelial stem cell , inflammation , biology , chlamydophila pneumoniae , cell adhesion molecule , endothelium , endothelial dysfunction , immunology , cell adhesion , vcam 1 , chlamydia , microbiology and biotechnology , cell , icam 1 , medicine , biochemistry , in vitro , endocrinology , environmental health , chlamydiaceae
Background 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. Materials and methods Endothelial intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1) and endothelial selectin (E‐selectin) expression were measured using flow cytometry, as an indication of endothelial activation. Cytotoxicity was monitored using the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay. Immunostaining was applied to measure Cp and CMV infectivity to endothelial cells. Results An increased number of infected endothelial cells in a monolayer population leads to a raised expression of adhesion molecules of the whole cell population, suggesting paracrine interactions. Iron additively up‐regulated Cp‐induced VCAM‐1 expression, whereas synergistically potentiated Cp‐induced ICAM‐1 expression. Together with CMV, iron also enhanced ICAM‐1 and VCAM‐1 expression. These iron effects were observed without modulation of the initial infectivity of both microorganisms. 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. Conclusions Endothelial response towards chronic infections depends on intracellular iron levels. Iron status in populations positive for Cp or CMV infections should be considered as a potential determinant for the development of atherosclerosis.