Association between eotaxin (CCL11), C-reactive protein, and antimicrobial antibodies in patients undergoing coronary angioplasty.
Eotaxin (CCL11) is a potent chemoattractant for eosinophils and lymphocytes. Apart from its functions in the eosinophilic system, eotaxin has been shown to be overexpressed in atherosclerosis. We therefore sought to determine whether chronic infection with Chlamydia pneumoniae or other infectious agents is correlated with concentrations of eotaxin or C-reactive protein since this mechanism could explain the finding that chronic infection stimulates smooth muscle cell migration and plaque development. Patients undergoing percutaneous coronary angioplasty (PCI) for acute coronary syndrome or stable angina were included in the study. Blood was drawn before PCI, at 6 weeks, and 6 and 12 months after coronary intervention. Eotaxin and C-reactive protein were determined by enzyme-linked immunosorbent assay (ELISA). Antibodies against Candida, C. pneumoniae, cytomegalovirus, Helicobacter pylori, and herpes simplex virus were measured by ELISA or immunofluorescence. Two hundred five consecutive patients undergoing PCI (stable angina, n = 136; acute coronary syndrome, n = 69) and 83 patients with normal coronary arteries were enrolled in the study. Eotaxin concentrations at inclusion were higher in patients with coronary artery disease than in control patients, p = .01, and comparable in patients with stable angina and those with acute coronary syndrome but did not correlate with C-reactive protein. Eotaxin concentrations at inclusion and during follow-up weakly correlated with concentrations of antibodies against C. pneumoniae, H. pylori, and herpes simplex virus but not with concentrations of antibodies against Candida or cytomegalovirus. Eotaxin concentrations and antibody titers against C. pneumoniae significantly increased following angioplasty and remained elevated thereafter. In conclusion, our data demonstrate that eotaxin concentrations are elevated independently from C-reactive protein in patients with coronary artery disease and correlate with antibodies against infectious agents known for chronic infection in humans.
Kaehler
Jan
J
Department of Cardiology, University Hospital Hamburg, Germany. kaehler@uke.uni-hamburg.de
Tuleweit
Anika
A
Steven
Daniel
D
Krempl
Tanja
T
Haar
Antje
A
Carstensen
Marion
M
Koester
Ralf
R
Terres
Wolfram
W
Meinertz
Thomas
T
D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000906:Antibodies / Q000097:blood; D000907:Antibodies, Bacterial / Q000097:blood; D000908:Antibodies, Fungal / Q000097:blood; D000914:Antibodies, Viral / Q000097:blood; D050197:Atherosclerosis / Q000209:etiology; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000097:blood*; D003324:Coronary Artery Disease / Q000097:blood / Q000209:etiology / Q000276:immunology; D005260:Female; D006801:Humans; D007239:Infections / Q000097:blood / Q000150:complications / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors
D000906:Antibodies; D000907:Antibodies, Bacterial; D000908:Antibodies, Fungal; D000914:Antibodies, Viral; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D002097:C-Reactive Protein