Human soluble tumor necrosis factor receptor I (sTNF-RI) and interleukin-I receptor antagonist (IL-I Ra) in different stages of acute rheumatic fever

• Published in: Anadolu kardiyoloji dergisi : AKD Vol. 8; no. 2; pp. 139 - 142
• Main Authors: Kütükçüler, Necil, Karaca, Neslihan E, Sözeri, Betül Y, Koturoğlu, Güldane, Kurugöl, Zafer, Ozyürek, Ruhi A, Aksu, Güzide
• Format: Journal Article
• Language: English
• Published: Turkey Aves Yayıncılık 01.04.2008
• Subjects: Acute Disease; Akut hastalık; Bacterial infections and mycoses; Bakteriyel enfeksiyonlar ve mikozlar; Cardiovascular diseases; Case-Control Studies; Child; Female; Hastalık şiddeti belirtileri; Humans; Kardiyovasküler hastalıklar; Male; Receptors, Interleukin-1; Receptors, Interleukin-1 - antagonists & inhibitors; Receptors, Tumor Necrosis Factor, Type I; Receptors, Tumor Necrosis Factor, Type I - blood; Reseptörler, interlökin-1; Reseptörler, tümör nekroz faktör, tip I; Rheumatic Heart Disease; Rheumatic Heart Disease - blood; Rheumatic Heart Disease - immunology; Rheumatic Heart Disease - pathology; Romatizmal kalp hastalığı; Severity of Illness Index
• ISSN: 1302-8723; 1308-0032

Acute rheumatic fever (ARF) results from an autoimmune response to infection with group A streptococci. Serum concentrations of two anti-inflammatory cytokines, interleukin-I receptor antagonist (IL-IRa) and human soluble tumor necrosis factor receptor I (sTNF-RI) were determined in patients with ARF at the time of admission and 3 months after treatment in order to evaluate changes in cytokine concentrations occurring during different stages of the disease. Serum concentrations of two anti-inflammatory cytokines, IL-I Ra and sTNF-RI , were investigated in children with ARF at the time of admission (n=21) and after 3 months following the cessation of treatment (n=15). The sTNF-RI and sIL-IRa were measured quantitatively in serum using enzyme-linked immunosorbent assay (ELISA). Levels of IL-1Ra and sTNF-RI were found to be significantly higher during acute phase and remission period of ARF when compared to age-matched healthy controls (p=0.001 and p=0.0001, respectively). Our study demonstrated that two anti-inflammatory cytokines, serum sTNFRI and IL-1Ra, are increased in acute and remission stages of ARF reflecting activation of the cellular immune response. We suggest this increase might probably be generated in an effort to counteract the already increased concentrations of proinflammatory cytokines.