Turk Kardiyol Dern Ars. 2022; 50(1): 14-21 | DOI: 10.5543/tkda.2022.77756
A study on the association of IL-10 promoter polymorphisms with rheumatic heart disease in Turkish female patients
Ayşegül Başak Akadam Teker1, Erhan Teker21Department of Medical Genetic, Giresun University Medical Faculty, Giresun, Turkey
2Clinic of Cardiology, Giresun University, A. İlhan Özdemir Training and Research Hospital, Giresun, Turkey
Objective: Rheumatic heart disease (RHD) is an inflammatory disease that develops following streptococcal infections. With the help of the pleiotropic effect, interleukin-10 (IL-10) has a role in regulating the responses of the immune system. However, impaired IL-10 expression or signal can impair antigen clearance during acute bacterial infections, creating a favorable environment for persistent inflammation. The aim of our study is to evaluate the relationship between variants' sensitivity of IL-10 (rs1800896, rs1800871, rs1800872) or severity of RHD in Turkish population.
Methods: In this case-control study, 390 female participants (170 RHD/220 control) were examined in terms of IL-10 rs1800896, rs1800871, rs1800872 using the TaqMan 5 'Allelic Discrimination Testing.
Results: It was found out that there was no statistically significant difference between study groups in terms of IL-10 rs1800896, rs1800871, rs1800872 genotypes. However, the rs1800896 variant made a statistically significant difference when both the group with combined valve lesions and the group with a single valve lesion were compared(χ 2=7.532,p=0.023), as well as the group with combined valve lesions and the control group(χ 2 =12.860, p=0.002).
Conclusion: The findings suggest that IL-10 rs1800896, rs1800871, rs1800872 variants are not associated with the pathogenesis of the disease in women in Turkish context. IL-10 rs1800896, rs1800871, rs1800872 variants Turkish population cannot be suggested as a suitable genetic marker for RHD. However, the IL-10 rs1800896 variant appears to be a risk factor for valve involvement. Further studies are needed to clarify the mechanism in this regard.
Keywords: IL-10, Polymorphism, Rheumatic Heart Disease, Rheumatic Fever
Corresponding Author: Ayşegül Başak Akadam Teker, Türkiye
Manuscript Language: Turkish