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

Abstract

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.

Trace element balance is changed in infected organs during acute Chlamydophila pneumoniae infection in mice

“…Measurements of Fe and Cu in atherosclerotic plaques have shown significantly higher concentrations of these elements as compared with the levels found in arterial samples from healthy individuals (Stadler et al 2004). Endothelial cell activation by C. pneumoniae infection has also been shown to be enhanced by Fe supplementation when compared with C. pneumoniae infection in cells not supplemented with Fe (Kartikasari et al 2006). Moreover, this Fe-induced activation could be reversed by Fe chelation.…”

Distribution of selected elements in atherosclerotic plaques of apoE/LDLR‐double knockout mice assessed by synchrotron radiation‐induced micro‐XRF spectrometry

“…17 In the light of inflammatory theory of atherogenesis, iron enhances endothelial cell activation in response to cytomegalovirus or Chlamydia pneumoniae infection. 18 A potential mechanism for arterial wall damage by iron involves modifications of LDL, the major carrier of blood cholesterol. Many lines of evidence suggest that LDL, an important risk factor for atherosclerosis, must be oxidatively modified to recruit and activate inflammatory and immune cells.…”

Iron overload and unique susceptibility of liver transplant recipients to disseminated disease due to opportunistic pathogens

“…Iron homeostasis is also important in the pathogenicity of CMV. Iron promotes endothelial cell activation in response to CMV infection, as indicated by the expression of the enhanced endothelial intercellular adhesion molecule 1 and the vascular adhesion molecule 68. Furthermore, iron chelators have antiviral and immunomodulatory activities and inhibit both CMV replication and endothelial cell surface molecule expression 69, 70.…”