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Aim : We examined the hypothesis that Chlamydia pneumoniae (CP) containing homologous HSP60 protein contributes to the triggering of autoimmune responses in atherosclerosis through anti-HSP60 antibodies. Methods and Results : The study cohort consisted of 151 consecutive ischemic heart disease patients. Anti-human (12%) and anti-chlamydial (23%) HSP60 antibodies were infrequent and not correlated. Anti-human HSP60 IgG related to CP IgG (p = 0.013), anti-Chlamydia HSP60 IgG did not. The presence and extent of coronary artery disease (CAD) was not associated with an antibody response to Chlamydia HSP60, human HSP60 or CP. Chlamydia HSP60 antibodies were decreased in patients with acute myocardial infarction (AMI; p = 0.032), anti-human HSP60 did not differ in patients with stable and unstable angina pectoris and AMI. Von Willebrand factor (vWf), soluble Vascular Cell Adhesion Molecule-1 (sVCAM-1) and flow-mediated vasodilatation were measured. sVCAM-1 correlated weakly with anti-chlamydial HSP60 (r = 0,163, p = 0,046). None of the other endothelial (dys)function markers correlated significantly to anti-chlamydial or anti-human HSP60 levels. Levels of significance of sVCAM-1 with CP titres >= 1:32, 1:64, 1:128, and 1:256 were 0.019, 0.010, 0.127, and 0.051 respectively. For flow-mediated vasodilatation of the brachial artery, p-values were 0.970, 0.281, 0.024, and 0.132. We did not find any association between the presence or absence of infection with CP and vWf regardless of the titer evaluated. Anti-HSP60 IgG levels did not correlate with CAD risk factors, anti-CP IgG associated with male sex and triglycerides. Conclusion : CAD was not associated with IgG antibodies against CP, Chlamydia HSP60, or human HSP60, arguing against the hypothesis that infection contributes to disease progression via anti-HSP antibodies and supplying additional evidence that CP is an unlikely CAD risk factor.
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J. Vasc. Biol. 42, Sup:2 (2005) p91