title: C(-260)T polymorphism in the promoter of CD 14 gene is not associated with myocardial infarction in the Tunisian population.
abstract: Recent findings suggest that inflammation plays a role in atherosclerosis and its acute complications. Several known mechanisms may play at least a partial role in this process. One of the most likely mechanisms involves lipopolysaccharide (LPS) and its receptor, CD14. The C(-260)T single nucleotide polymorphism (rs2569190) in the promoter region of the CD14 receptor gene has been reported to be associated with a higher risk of MI. Others studies, however, have not corroborated these findings. Considering the contradictory results, the aim of the present study was to investigate the possible association between the CD14 C(-260)T polymorphism and the risk of MI in the Tunisian population. A total of 321 Tunisian patients with MI and 344 healthy controls were included in the study. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. The frequency of TT homozygous genotype for the CD14 C(-260)T polymorphism was 26.2% in MI patients and 27.0% in the control group. However, the genotype distribution and allele frequencies were not significantly different between MI and controls subjects. Moreover, the odds ratio for MI associated with the TT genotype failed to reach statistical significance (OR=1.22; 95% CI: 0.85-1.77; p=0.272). These results do not support the hypothesis that the C-260T polymorphism of CD14 gene contributes to the genetic susceptibility to MI in the Tunisian population studied.
authors.affiliation: Research Laboratory LR99ES11, Department of Biochemistry, Tunisia.
authors.forename: Yousra
authors.initials: Y
authors.lastname: Sediri
authors.forename: Sabrine
authors.initials: S
authors.lastname: Hammami
authors.forename: Amani
authors.initials: A
authors.lastname: Kallel
authors.forename: Mohamed Sami
authors.initials: MS
authors.lastname: Mourali
authors.forename: Moncef
authors.initials: M
authors.lastname: Feki
authors.forename: Monia
authors.initials: M
authors.lastname: Elasmi
authors.forename: Sameh
authors.initials: S
authors.lastname: Haj-Taieb
authors.forename: Souheil
authors.initials: S
authors.lastname: Omar
authors.forename: Haïfa
authors.initials: H
authors.lastname: Sanhaji
authors.forename: Rachid
authors.initials: R
authors.lastname: Mechmeche
authors.forename: Riadh
authors.initials: R
authors.lastname: Jemaa
authors.forename: Naziha
authors.initials: N
authors.lastname: Kaabachi
mesh_terms: D016022:Case-Control Studies; D004273:DNA, Neoplasm / Q000235:genetics; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011379:Prognosis; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012307:Risk Factors; D014416:Tunisia / Q000453:epidemiology
chemical_list: D004273:DNA, Neoplasm; D018950:Lipopolysaccharide Receptors