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.

A randomized trial in patients undergoing percutaneous coronary angioplasty: roxithromycin does not reduce clinical restenosis but angioplasty increases antibody concentrations against Chlamydia pneumoniae.

BACKGROUND: Elevated antibodies against Chlamydia pneumoniae have been associated with coronary artery disease. In patients undergoing percutaneous coronary angioplasty, we therefore investigated the effect of roxithromycin on symptomatic restenosis and determined antichlamydial antibodies as well as inflammatory and immunological parameters. METHODS: A total of 327 patients undergoing coronary angioplasty were randomized to roxithromycin or placebo and followed-up for 1 year. Antibodies were determined by microimmunofluorescence and enzyme-linked immunosorbent assay; C-reactive protein, interleukin-10, tumor necrosis factor-alpha (TNF-alpha), and eotaxin were determined by enzyme-linked immunosorbent assay. RESULTS: Although the frequency of restenosis was not affected by roxithromycin (25 restenoses vs 32 in the control group), antichlamydial antibodies increased during follow-up (anti-CP IgG +12 +/- 2%, P < .001). Concentrations of TNF-alpha and eotaxin increased as well (TNF-alpha +9 +/- 1% and eotaxin +10 +/- 2%) and correlated with antichlamydial antibody concentrations (TNF-alpha, r = 0.23, P = .02; eotaxin, r = 0.32, P = .002). CONCLUSIONS: Treatment with roxithromycin was not associated with a reduction of symptomatic restenoses. During follow-up, a marked increase in antichlamydial antibodies, TNF-alpha, and eotaxin was observed, suggesting that angioplasty-induced plaque rupture induces a specific immunological response without activation of inflammatory mechanisms as represented by C-reactive protein. Whether this mechanism occurs in all plaque ruptures remains to be determined.