The effects of interleukin (IL)1, 6, 10 and tumor necrosis factor (TNF) gene polymorphisms on CRP levels in coronary artery disease

Abstract

Atherosclerosis is a dynamic and progressing inflammatory pathology. Studies have demonstrated that genetic variants that directly or indirectly alter the inflammatory system raise the risk of coronary artery disease (CAD). Genetic variations account for the variances in how the disease develops and progresses as well as the disclosure of poor prognostic information linked to extreme inflammatory reactions in individuals. In our investigation, we aimed to determine whether there may be a connection between CAD and the IL-1 C-889T, IL-6 G-174C, IL-10 G-1082A, and TNF G-308A polymorphisms. In the study, 80 patients with coronary artery stenosis of 70% or more and 80 people with normal coronary arteries were both evaluated using coronary angiography. An enzymatic colorimetric approach was used to quantify fasting blood glucose (FBG), the serum lipid profile, and an immunoturbidimetric method was used to measure CRP levels. Real-time PCR was used to identify IL-1 C-889T, IL-6 G-174C, IL-10 G1082A, and TNF G-308A polymorphisms. CRP (mg/L) levels varied in the CAD group for IL-1 C-889T and IL-10 G-1082A (p = 0.031 and 0.018, respectively). For IL-1, wild (CC) type CRP levels were 18.93 16.38, mutant (TT) genotype CRP levels were 53.12 21.03, and wild (GG) type CRP levels were 23.09 16.64. As a result, it was discovered that atherosclerosis significantly depends on the balance between pro and anti-inflammatory cytokines. In the presence of mutations in these cytokines, we identified variations in the levels of inflammatory markers.