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CLINICAL STUDY

CD14 C(-260)T polymorphism, plasma levels of the soluble endotoxin receptor CD14, their association with chronic infections and risk of stable coronary artery disease

Wolfgang Koenig, MD, FACC^*, Natalie Khuseyinova, MD^*, Michael M. Hoffmann, PhD, Winfried März, MD, Margit Fröhlich, MD^*, Albrecht Hoffmeister, MD^*, Hermann Brenner, MD, MPH and Dietrich Rothenbacher, MD, MPH^,*

^* Department of Internal Medicine II-Cardiology, University of Ulm Medical Center, Ulm, Germany
Department of Clinical Chemistry, University of Freiburg, Freiburg, Germany
Department of Epidemiology, University of Ulm, Ulm, Germany
Department of Epidemiology, the German Centre for Research on Ageing, University of Heidelberg, Heidelberg, Germany

Manuscript received January 16, 2002; revised manuscript received March 14, 2002, accepted March 27, 2002.

^* Reprint requests and correspondence: Dr. Dietrich Rothenbacher, Department of Epidemiology, German Centre for Research on Ageing, Bergheimerstr. 20, D-69115 Heidelberg, Germany.
rothenbacher{at}dzfa.uni-heidelberg.de

OBJECTIVES: We sought to investigate the association of CD14 genotype and plasma levels of soluble (s)CD14 with risk of stable coronary artery disease (CAD), chronic infections and sensitive markers of systemic inflammation.

BACKGROUND: It has been suggested that genetic variation of the CD14 receptor with increased CD14 gene expression might play a role in atherogenesis. A mechanistic link would consist in its contribution to the inflammatory response seen in this disease.

METHODS: We measured levels of sCD14 (µg/ml; ELISA) in 312 patients with angiographically proven CAD and stable angina pectoris, and in 477 age- and gender-matched healthy blood donors. CD14 genotype was determined by polymerase chain reaction. In addition, seropositivity to Chlamydia pneumoniae and Helicobacter pylori, a complete lipid profile and various sensitive systemic markers of inflammation were measured.

RESULTS: CD14 C(-260)T genotype was not independently associated with increased risk of CAD after multivariable adjustments (odds ratio [OR] 1.34; 95% confidence interval [CI] 0.84 to 2.16). However, sCD14 plasma levels were higher in subjects with TT genotype compared with those with CT or CC genotype (p = 0.005). Plasma levels were not different between cases and controls (4.2 ± 1.3 µg/ml vs. 4.3 ± 1.3 µg/ml, p = NS). In multivariable logistic regression, the OR for the presence of CAD was 1.11 (95% CI, 0.65 to 1.91) if the top quintile of the sCD14 distribution was compared with the bottom quintile. There was no consistent association between seropositivity to either C. pneumoniae or H. pylori, or both, and sCD14 levels and between sCD14 levels or CD14 genotype and the various markers of inflammation.

CONCLUSIONS: These results do not confirm an independent relationship between CD14 genotypes or plasma levels of sCD14 and risk of stable CAD in this population.

Abbreviations and Acronyms   AMI   acute myocardial infarction   BMI   body mass index   CAD   coronary artery disease   CI   confidence interval   CRP   C-reactive protein   EC   endothelial cell   HDL   high-density lipoprotein   ICAM   intercellular adhesion molecule   IL   interleukin   LDL   low-density lipoprotein   Lp(a)   lipoprotein (a)   LPS   lipopolysaccharide   mCD14   membrane-bound CD14   NO   nitric oxide   OR   odds ratio   PAI   plasminogen-activator inhibitor   PCR   polymerase chain reaction   SAA   serum amyloid A   sCD14   soluble CD14   SMC   smooth muscle cell   TNF   tumor necrosis factor   vWF   von Willebrand factor

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