A relationship between serological markers of chronic C. pneumoniae and CMV infection and hsp60 in patients with atherosclerotic carotid stenosis.
AbstractA number of epidemiological studies conducted over the last decade indicate a relationship between specific pathogen infections and the development of atherosclerosis, although no pathogenetic pathways connecting these two have been determined. Recent reports support the role of heat shock proteins (HSPs) in atherogenesis. The HSPs are also believed to be a link between the infection and the development of atherosclerotic lesions. THE AIMS OF STUDY: Immunohistochemical evaluation of carotid artery segments to show the relationship between the presence of heat shock proteins and the serum levels of anti-hsp60 antibodies. An attempt to demonstrate a relationship between an expression of chronic C. pneumoniae and CMV antigens. The study included 41 patients qualified for carotid artery endarterectomy and 18 healthy volunteers of corresponding age. Levels of anti- hsp60, anti-C. pneumoniae IgA and IgG, anti-CMV IgG antibodies as well as hsCRP were determined. The mean serum levels of anti-hsp60 antibodies were higher in patients with advanced atherosclerosis as compared to healthy volunteers (55.3 ± 64.1 vs 32.8 ± 29.8; p < 0.05). There was a strong correlation between anti-hsp60 antibodies and the expression of hsp60 in carotid arterial wall, as confirmed by immunohistochemical evaluation. The study group showed statistically significant higher levels of hsCRP. Furthermore, statistically significant higher serum levels of anti-C. pneumoniae IgG and IgA as well as anti-CMV IgG antibodies were found in the study group as compared to controls. No correlation was shown between the markers of chronic infection induced by the tested pathogens and serum levels of anti-HSP and hsCRP. Higher protein expression in vascular walls is closely correlated with the level of anti-hsp60. At the same time, no significant relationship between anti-hsp60 antibodies and serological markers of infection was observed, which may only indicate an indirect role of infection in the assessment of breaking the immunological tolerance against autologous HSPs.
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