Interleukin-18 Gene Polymorphism in Patients with and without Atherosclerotic Coronary Artery Disease

Loading...
Thumbnail Image

Journal Title

Journal ISSN

Volume Title

Publisher

Shiraz University of Medical Sciences

Abstract

Background:Several studies have revealed that inflammation plays an important role in development of Coronary Artery Disease (CAD) and its other manifestations. IL-18 is a pleiotropic cytokine that enhances Th1( T helper 1) or Th2( T helper 2) immune response depending on its cytokine milieu and genetic background. It strongly induces formation of plaques in patients with CAD. Variations in the IL-18 gene found to influence both levels of IL-18 and clinical outcomes in individuals with history of heart disease. To investigate the association of two IL-18 promoter gene polymorphisms at -607C/A and -137G/C positions with CAD, and some CAD risk factors such as diabetes, arterial hypertension, hypercholesterolemia, cigarette smoking and obesity.Methods: Genomic DNA was extracted by the salting out method from the peripheral arterial blood of 280 patients with CAD documented by coronary angiography (143 with a documented history of myocardial infarction termed positive MI and 137 without myocardial infarction designated negative MI) and 140 age- sex matched persons with a normal coronary angiography (control group).The genotype of both CAD and control groups were assessed by ASP-PCR method. Arlequin program was used for gametic phase estimation and haplotype analysis.Results: There was no significant difference between patient and control groups either allelic, genotypic, and haplotypic for both variants (p>0.05). Furthermore, no significant correlation was found between IL-18 genotypes and CAD risk factors in the patient group (P>0.05).Conclusion: These results suggest that the investigated IL-18 gene promoter polymorphisms at -607C/A and -137G/C positions are not associated with genetic susceptibility to CAD in southern Iran.

Description

Keywords

Citation

URI

Endorsement

Review

Supplemented By

Referenced By