Investigation of interleukin-17 Gene-152g/A polymorphism and IL-17 Serum levels in patients with cardiac syndrome X
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CitationÖzer, Y. G., Önal, B., Özen, D., Kandaz, C., & Demir, B. (2018). Kardiyak Sendrom X Hastalarinda İnterlökin-17 Serum Seviyesi ve Il-17 Geni-152g/A Polimorfizminin Araştirilmasi. Journal of Academic Research in Medicine, 8(3).
Objective: Cardiac syndrome X (CSX) can be defined as experiencing chest pain with angina by patients with normal coronary arteries. Endothelial and microvascular dysfunction is responsible for the pathophysiology of the inflammatory CSX disease. Inflammation is especially an important factor in the progression of ischemic heart diseases. It is accepted that both the number of B and T lymphocytes and expression of various proinflammatory cytokines released from those cells increases during inflammatory response. Different proinflammatory cytokines are produced by activated macrophages and T lymphocytes. Since interleukin-17 (IL-17) induces many signaling molecules, which promote immune response and play a role in inflammation, it is assumed that IL-17 can play a role in the CSX pathogenesis. In our study, the relationship between CSX and IL-17 serum levels and the -152G/A polymorphism on IL-17 gene was investigated. Methods: Serum IL-17 levels of blood samples were analyzed from 100 patients with CSX and 101 healthy control individuals using the Enzyme-Linked ImmunoSorbent Assay (ELISA) method. After the DNA isolation was performed from blood samples, the IL-17 gene-152G/A polymorphisms were detected based on the PCR-RFLP method for both patients and healthy individuals. The pomotor region of the IL-17 gene was amplified by the PCR method, and then, genotyping was performed using PCR products for the RFLP step. After that, obtained data for CSX patients and the healthy control group were compared using the statistical analysis. Results: When the IL-17 gene-152G/A polymorphism genotyping results of patients with CSX and healthy control individuals were compared, no statistically significant difference was observed in both genotypic and allelic distributions (p=0.218). The IL-17 serum levels were found to be significantly higher in patients with CSX than in healthy controls (p<0.001). Conclusion: Endothelium plays a significant role in the regulation of vascular functions. Inflammatory response is generated against the endothelial activation in the CSX pathogenesis. An increase in the CRP levels, which is a marker of inflammation, is common for both coronary artery disease and CSX, associated with endothelial dysfunction. Helper T cells play important roles in cardiovascular diseases. IL-17 induces the expression of different proinflammatory cytokines and chemokines, participating in the tissue infiltration and destruction. There are also several studies that prove the significant role of proinflammatory IL-17, which is released from T cells, in cardiovascular diseases, supporting our results. In addition, it has been demonstrated that statins, having anti-inflammatory effects, inhibit the IL-17 gene expression and cytokine release. In this context, we foresee that statins can have a subsidiary effect on the CSX treatment to suppress the inflammatory response in patients in who the IL-17 levels were determined as significantly higher than in healthy controls.