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.
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.
Authors: Lee Ann Campbell; Kambiz Yaraei; Brian Van Lenten; Alan Chait; Erwin Blessing; Cho-Chou Kuo; Tadayoshi Nosaka; Jerry Ricks; Michael E Rosenfeld Journal: Microbes Infect Date: 2010-04-22 Impact factor: 2.700
Authors: Geoffrey T L Kloppenburg; Rick de Graaf; Gert E L M Grauls; Cathrien A Bruggeman; Frank R Stassen Journal: BMC Microbiol Date: 2007-12-06 Impact factor: 3.605