C(− 260)T polymorphism in the promoter of CD 14 gene is not associated with myocardial infarction in the Tunisian population

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.

Research Highlights
► In this case-control study, the participants included 344 unrelated male patients with MI and 321 healthy subjects.
► We investigated the association between the C(− 260)T polymorphism in the promoter of CD14 gene and MI in the Tunisian population.
► The polymorphism C(− 260) T was determined in all participants by a polymerase chain-reaction-restriction fragment length polymorphism assay (PCR-RFLP).
► The genotype distribution and allele frequencies were not significantly different between MI and controls subjects.