Does infection with chlamydia pneumoniae and/or helicobacter pylori increase the expression of endothelial cell adhesion molecules in humans?

Chlamydia LPS and MOMP seropositivity are associated with different cytokine profiles in patients with coronary heart disease

“…In a previous publication we have demonstrated that the antibody profile with regard to C. pneumoniae MOMP antibodies and Chlamydia LPS antibodies differ between individuals and that this difference cannot be explained by antibodies to the other human chlamydiae, Chlamydia trachomatis and Chlamydia psittaci [13]. We could also show an association between the presence of Chlamydia LPS IgA antibodies and some proinflammatory variables in CHD patients [24,25]. To further study the association between the Chlamydia antibody profile and certain cytokine patterns, we included IFN γ and IL-10 as they are suggested to be of crucial importance for the outcome of Chlamydia infections [26][27][28].…”

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

“…Chlamydia pneumoniae (Cp), the gram-negative obligate intracellular bacterium, is capable of infecting endothelial cells [7][8][9][10] as well as inducing the expression of adhesion molecules on these cells [11,12]. Cp infection also leads to increased soluble adhesion molecules in human [13]. Differential induction of adhesion molecule expression by cytomegalovirus (CMV) has also been demonstrated [14 -18].…”