Kardiyak Sendrom X Hastalarinda İnterlökin-17 Serum Seviyesi ve Il-17 Geni-152g/A Polimorfizminin Araştirilmasi.

Objective: Cardiac Syndrome X (CSX) can be defined as having chest pain with angina in patients with normal coronary arteries. Endothelial and microvascular dysfunction is responsible from pathophysiology of the inflammatory CSX disease. Inflammation is an important factor for progression of especially ischemic heart diseases. It is accepted that both number of B and T lymphocytes and expression of various proinflammatory cytokines that are released from those cells increase during inflammatory response. Different proinflammatory cytokines are produced by activated mcrophages and T lymphocytes. Since interleukin-17 (IL-17) induces many signaling molecules, which promote immune response and have role in inflammation, it is assumed that IL-17 can play a role in pathogenesis of CSX. In our study, the relation of CSX with IL-17 serum levels and - 152G/A polymorphism on IL-17 gene was investigated. Methods: Serum IL-17 levels of blood samples from 100 CSX patients and 101 healthy control individuals by using ELISA method. After DNA isolation was performed from blood samples, IL-17 gene -152G/A polymorphisms were detected based on PCR-RFLP method for both patients and healthy individuals. Promotor region of IL-17 gene was amplified by PCR method and then, genotyping was performed by using PCR products for RFLP step. After that, obtained data for CSX patients and healthy control group were compared by statistical analysis. Results: When IL-17 gene -152G/A polymorphism genotyping results of CSX patients and healthy control individuals were compared, no statistically significant difference was observed in both genotypic and allelic distributions (p=0.218). IL-17 serum levels were found as statistically significantly higher in CSX patients than healthy controls (p<0.001). Conclusion: Endothelium has significant role in regulation of vascular functions. Inflammatory response is generated against endothelial activation in the pathogenesis of CSX. Increase in CRP levels, which is a marker of inflammation, is a common for both coronary artery disease and CSX, associated with endothelial dysfunction. Helper T cells take important parts in cardiovascular diseases. IL-17 induces expression of different proinflammatory cytokines and chemokines, participating in 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. Besides, it has been demonstrated that statins, having anti-inflammatory effects, inhibit IL-17 gene expression and cytokine release. In this context, we foresee that statins can have a subsidiary effect on CSX treatment to suppress inflammatory response in patients, of which IL-17 levels were determined as significantly higher than healthy controls. [ABSTRACT FROM AUTHOR]