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

Abstract

Abstract Objective To investigate if Chlamydia pneumoniae and/or Helicobacter pylori seropositivity is associated with elevated levels of soluble endothelial cell adhesion molecules (sCAMs) as markers of atherosclerotic activity. Methods Immunoglobulin A (IgA) and IgG antibodies to the two bacteria, soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and E-selectin were measured in coronary heart disease (CHD) patients ( n = 193) and age- and sex-matched controls ( n = 193). Two different serological methods were used for the detection of Chlamydia antibodies: Labsystems microimmunofluorescence to detect species-specific C. pneumoniae antibodies and Medac's recombinant enzyme-linked immunosorbent assay to detect genus-specific lipopolysaccharide antibodies. Results The concentrations of sICAM-1 and E-selectin were higher in CHD patients with positive vs. negative Chlamydia lipopolysaccharide IgA ( P = 0.044 for both). H. pylori antibodies alone did not predict raised levels of sCAMs, but in CHD patients sICAM-1 was increased with IgA seropositivity to both bacteria compared to double seronegativity ( P = 0.034). Concentrations of sVCAM-1 were elevated in CHD patients with double IgA seropositivity compared to those with Chlamydia lipopolysaccharide IgA seropositivity alone ( P = 0.018). Conclusion Our results may indicate that C. pneumoniae contributes to increased inflammation in CHD, and that this contribution is even more pronounced when present in combination with H. pylori IgA antibodies.