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

authors:

avatar Alireza Abdi ardekani 1 , avatar S Shayan 1 , * , avatar Mohammad Javad Zibaeenezhad 1 , avatar MR Haghshenas 2 , avatar N Erfani 2 , avatar A Ghaderi 2

Cardiovascular Research Center, Shiraz University of Medical Scinces, Shiraz, Iran
Shiraz Institute for Cancer Research, Shiraz University of Medical Scinces, Shiraz, Iran

how to cite: Abdi ardekani A, Shayan S , Zibaeenezhad M J , Haghshenas M , Erfani N , et al. Interleukin-18 Gene Polymorphism in Patients with and without Atherosclerotic Coronary Artery Disease. Int Cardiovasc Res J. 2009;3(3):e68041. 

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.

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References

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