Abstract
IL-1RA is a member of the interleukin-1 cytokine family. IL1Ra is secreted by various types of cells, including immune cells, epithelial cells, and adipocytes, and is a natural inhibitor of the pro-inflammatory effect of IL1. This protein inhibits the activity of interleukin 1, alpha (IL1A) and interleukin 1, beta (IL1B) and modulates various interleukin 1-related immune and inflammatory responses. Hypothesis: The aim of this study was to investigate the relationship between IL1RN gene polymorphism and the development of acute myocardial infarction (AMI) in young patients. Material/methods: In a case-control study, we investigated polymorphisms in the IL1RN gene (rs4251961) using quantitative real-time polymerase chain reaction analysis. The study was conducted with AMI (age range: 36 to 55 years; mean: 42.74 ± 12.47 years) with 11 healthy people in the control group. We also studied the interaction between genetic polymorphism and inflammatory agents such as CRP, IL 1, IL 6. All indicators were calculated using the statistical program Statistica 12.0, a P-value <0.05 was considered statistically significant. Results: Statistically significant differences in the distribution of rs4251961 genotypes were observed between the two groups. Carriers of the T allele had a significantly higher risk of developing AMI than carriers of the C allele (P <0.05). Subjects carrying the TT and TC haplotypes have a significantly increased incidence of coronary artery disease. We also found that the CYP1B1 rs1056836 polymorphism had a synergistic effect with CRP levels on the risk of coronary heart disease. Conclusions: The rs4251961 gene polymorphism is closely associated with the development of AMI in patients with coronary artery disease. There is a mutual synergistic effect between the inflammatory response and IL1RN gene polymorphism in relation to the development of CAD complications. Functional polymorphisms of the IL1RN gene can affect the susceptibility and progression of CAD, increase the pro-inflammatory response, and destabilize the atherosclerotic plaque.
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