Abstract
Objective— Chlamydia pneumoniae (Cpn) infection of vascular smooth muscle cells increases interleukin-6 (IL-6) secretion in vitro. In vivo, IL-6 stimulates liver C-reactive protein (CRP) production. Because serum levels of IL-6 and CRP are independent risk factors for stroke and myocardial infarction (MI), we investigated whether Cpn burden in carotid plaques might provide a link between plaque IL-6 expression and elevated serum levels of IL-6 and CRP. Methods and Results— Consecutive patients undergoing elective carotid endarterectomy were studied. Serum levels of CRP and IL-6 were measured before surgery. Immunohistochemistry and real-time quantitative (k)RT-PCR were used to detect Cpn and the expression of IL-6 within carotid plaques. Cpn mRNA was present in 19 (37%) of 51 patients, suggesting viable infections. These patients had evidence for infection by PCR and immunohistochemistry. The Cpn burden, measured by real-time quantitative (k)-PCR using the number of organisms normalized against the number of eukaryotic cells in the tissue, was associated with plaque expression of IL-6 (Spearman R =0.55; P <0.0001), which was associated with serum levels of IL-6 ( R =0.56; P <0.0001) and CRP ( R =0.80; P <0.0001). Conclusions— IL-6 secretion in atherosclerotic plaques infected with Cpn could explain elevated serum inflammatory markers in individuals at risk for stroke and MI. Serum interleukin-6 (IL-6) and C-reactive protein (CRP) are risk factors for stroke. Carotid plaque Chlamydia pneumoniae (Cpn) burden may contribute to these factors. Burden was significantly associated with IL-6 plaque expression, which was associated with serum IL-6 and CRP. Cpn is associated with inflammation and atherogenesis via upregulation of local and systemic inflammatory markers.