title: CD14 and IL6 polymorphisms are associated with a pro-atherogenic profile in young adults with acute myocardial infarction.
abstract: This study investigated the relationship of polymorphisms in genes encoding CD14, IL-6 and TLR4 with metabolic, inflammatory and endothelial markers in young adults with acute myocardial infarction (AMI). Glucose, lipids, nitrate and inflammatory markers, flow mediated vasodilatation (FMV) and flow mediated by nitrate (FMN) were evaluated in 102 AMI and 108 non-AMI (control group) young individuals (<45 years). CD14 -260C>T (rs2569190), IL6 -174G>C (rs1800795) and TLR4 c.896A>G (rs4986790) and TLR4 c.1196C>T (rs4986791) polymorphisms were analyzed by PCR-RFLP. Minor allele frequencies of CD14, IL6 and TLR4 polymorphisms were similar between AMI and control groups (p > 0.05). In AMI group, individuals carrying IL6 -174CC genotype had higher serum triglycerides, VLDL cholesterol and glucose compared to the IL6 -174GG/GC genotype carriers (p < 0.05). Multiple logistic analysis showed that IL6 -174CC genotype carriers had increased risk for hyperglycemia (>5.77 mmol/l) [OR: 6.75, 95 % CI: 1.80-24.40, p = 0.004] and hypertriglyceridemia (>2.68 mmol/l) [OR: 3.00, 95 % CI: 1.00-9.00, p = 0.043]. Moreover, CD14 -260TT genotype was associated with reduced serum HDL cholesterol [OR: 3.10, 95 % CI: 1.00-9.01, p = 0.044] and apolipoprotein AI [OR: 3.20, 95 % CI: 1.00-9.70, p = 0.038] in AMI group. Relationship between CD14 and IL6 variants and altered inflammatory and endothelial (nitrate, FMV and FMN) markers was not found in both AMI and control groups. The IL6 -174G>C and CD14 -260C>T polymorphisms are likely to be associated with a pro-atherogenic profile but not with increased inflammatory markers and endothelial dysfunction in young AMI patients.
authors.affiliation: Department of Clinical Analysis and Toxicology, Faculdade de Ciencias Farmaceuticas, School of Pharmaceutical Sciences, University of Sao Paulo, Av. Prof. Lineu Prestes, 580, B.17, São Paulo, SP, 05508900, Brazil, lidio@usp.br.
authors.forename: Lidio Gonçalves
authors.initials: LG
authors.lastname: Lima-Neto
authors.forename: Rosario Dominguez Crespo
authors.initials: RD
authors.lastname: Hirata
authors.forename: André Ducati
authors.initials: AD
authors.lastname: Luchessi
authors.forename: Vivian Nogueira
authors.initials: VN
authors.lastname: Silbiger
authors.forename: Marco Antonio
authors.initials: MA
authors.lastname: Stephano
authors.forename: Marcelo Ferraz
authors.initials: MF
authors.lastname: Sampaio
authors.forename: Dikran
authors.initials: D
authors.lastname: Armaganijan
authors.forename: Mario Hiroyuki
authors.initials: MH
authors.lastname: Hirata
mesh_terms: D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000097:blood / Q000235:genetics* / Q000503:physiopathology; D005260:Female; D005838:Genotype; D006801:Humans; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics*; D008055:Lipids / Q000097:blood; D018950:Lipopolysaccharide Receptors / Q000097:blood / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000235:genetics* / Q000503:physiopathology; D011110:Polymorphism, Genetic; D051197:Toll-Like Receptor 4 / Q000097:blood / Q000235:genetics
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D008055:Lipids; D018950:Lipopolysaccharide Receptors; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4