Abstract

Aim. Acute rheumatic fever is an inflammatory disease developing after upper respiratory tract infection with group A streptoccoci and its most important complication is rheumatic heart disease (RHD). Tumor necrosis factor (TNF)-α and interleukin (IL) –1–1082 gene polymorphisms were associated with susceptibility to develop rheumatic heart disease. The aim of our study is to determine the frequency of IL-10–1082 A/G and TNF-α-308 G/A gene polymorphism in Turkish population and to investigate the relationship between these polymorphisms and rheumatic heart disease. Material and Methods. Genotypes of 57 unrelated children with rheumatic heart disease and 99 controls were determined by use of PCR-RFLP. Results. No significant differences were found in genotypes or allele frequencies of TNF-α-308 and IL-10–1082 genes between RHD and control group. There was no relation between TNF-α-308 genotype and allel distribution with valvular involvement (p>0.05). IL-10–1082 GG and AG genotypes were seen more frequent in patients with multiple valvular disease but there was no statistical significance (p>0.05). Conclusion. As a result, there was no relationship between TNF-α-308, IL-10– 1082 gene polymorphisms and rheumatic heart disease or valvular involvement in the study population (p>0,05). Our results are thought that TNF-α-308 polymorphisms are silent and may become important only with some certain HLA allels. Further studies checking both cytokine polymorphism and HLA allels are needed.

Highlights

  • Rheumatic heart disease (RHD) is an inflammatory disorder and autoimmune sequel of group A streptococcal infection complicated by rheumatic fever (RF)

  • The aim of our study is to find out the possible influences of IL-10–1082 A/G and tumor necrosis factor (TNF)-α-308 G/A gene polymorphisms on RHD development

  • Clinical characteristics Our study population consisted of 57 RHD patients (27 female, 30 male) and 99 age-matched healthy control subjects (43 female, 56 male) without a history of heart failure

Read more

Summary

Introduction

Rheumatic heart disease (RHD) is an inflammatory disorder and autoimmune sequel of group A streptococcal infection complicated by rheumatic fever (RF). Autoimmunity induced by antigenic mimicry between the streptococcal glycoprotein and human cardiac miyosin may be responsible for the pathogenesis of RHD [1]. High familial incidence of RF suggests that genetic factors play a role in susceptibility to RF and RHD. Cytokines appear to play a critical role in triggering inflammatory and immunologic reactions in RF. Increase in tumor necrosis factor (TNF) -α and interleukin (IL) –1 levels in patients with RF and RHD have been known for a long time [3]. The biological actions are mainly inhibitory including inhibition of pro-inflammatory cytokines [5]

Objectives
Methods
Results

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.