S. Claiborne Johnston1,2, Hui Zhang1,2, Louis M. Messina1,2, Michael T. Lawton1,2, Deborah Dean1,2
1Children's Hospital Oakland Research Institute (H.Z., D.D.), California.
2From the Department of Neurology (S.C.J., M.T.L.), Division of Vascular Surgery, Department of Surgery (L.M.M.), and Department of Medicine (D.D.), University of California, San Francisco; and Children’s Hospital Oakland Research Institute (H.Z., D.D.), California.
Tóm tắt
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.
