title: Interleukin-6-572C>G polymorphism-association with inflammatory variables in Korean men with coronary artery disease.
abstract: Growing evidence suggests that polymorphisms at position -174 and -572 in interleukin-6 (IL-6) gene are associated with various manifestations of atherosclerosis. We investigated the genotype effects of IL-6 -174 and -572 polymorphisms on circulating levels of inflammatory markers in Korean men with coronary artery disease (CAD). CAD patients were subdivided into 2 groups; those patients treated without lipid-lowering drug (LLD) (n = 173) and those treated with LLD (n = 353). No significant differences existed between the 2 groups in age, body mass index, blood pressure, serum glucose, alcohol consumption, cigarette smoking, and the proportions of antihypertensive and antiplatelet therapies. IL-6 - 572 C>G polymorphism was only observed in this population. In CAD patients not taking LLD, the G/G genotype of the -572C>G polymorphism was associated with greater concentrations of IL-6 (C/C: 4.1 +/- 0.8 pg/mL, C/G: 3.7 +/- 0.7, G/G: 12.4 +/- 6.6; P = 0.031), C-reactive protein (CRP) (C/C: 1.9 +/- 0.4 mg/dL, C/G: 2.7 +/- 0.8, G/G: 10.1 +/- 3.9; P = 0.002), fibrinogen (C/C: 334 +/- 6 mg/dL, C/G: 345 +/- 13, G/G: 429 +/- 38; P = 0.003), and oxidized low-density lipoprotein (ox-LDL) (C/C: 59 +/- 2 mg/dL, C/G: 55 +/- 3, G/G: 71 +/- 6; P = 0.041) than those with C/C or C/G. However, in the LLD group, no difference existed in circulating levels of IL-6, CRP, fibrinogen, and ox-LDL across the genotype after adjustment of age. This study suggests that circulating levels of IL-6 and its related proteins such as CRP and fibrinogen are associated with genotype at a promoter polymorphism (-572C>G) of the IL-6 gene in Korean men with CAD not taking LLD. LLD, mostly statin in this study, might reduce the exaggeration of G/G genotype-raising effect on inflammatory markers.
authors.affiliation: Cardiovascular Genome Center, Yonsei University, Seoul, Korea.
authors.forename: Yangsoo
authors.initials: Y
authors.lastname: Jang
authors.forename: Oh Yoen
authors.initials: OY
authors.lastname: Kim
authors.forename: Yae Jung
authors.initials: YJ
authors.lastname: Hyun
authors.forename: Jey Sook
authors.initials: JS
authors.lastname: Chae
authors.forename: Soo Jeong
authors.initials: SJ
authors.lastname: Koh
authors.forename: Yu Mi
authors.initials: YM
authors.lastname: Heo
authors.forename: Donghoon
authors.initials: D
authors.lastname: Choi
authors.forename: Dong-Jik
authors.initials: DJ
authors.lastname: Shin
authors.forename: Kenneth
authors.initials: K
authors.lastname: Huttner
authors.forename: Jong Ho
authors.initials: JH
authors.lastname: Lee
mesh_terms: D000328:Adult; D044466:Asian People / Q000235:genetics; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D003324:Coronary Artery Disease / Q000097:blood* / Q000453:epidemiology / Q000235:genetics*; D005340:Fibrinogen / Q000032:analysis; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006949:Hyperlipidemias / Q000188:drug therapy / Q000453:epidemiology / Q000235:genetics; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood* / Q000235:genetics*; D007723:Korea / Q000453:epidemiology; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000235:genetics; D012016:Reference Values
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D015850:Interleukin-6; D008055:Lipids; D005340:Fibrinogen; D002097:C-Reactive Protein