Serum Concentrations of Interleukin-33 and its Soluble Receptor sST2 in Patients with Persistent Atrial Fibrillation
- *Corresponding Author:
- Wael Alkhiary
Department of Clinical Pathology, Hematology Division
Hemostasis and Thrombosis Laboratory, Mansoura University
Tel: +2 01113228256
Fax: +20 50 2245451
E-mail: [email protected]
Received Date: Apr 10, 2015; Accepted Date: May 28, 2015; Published Date: May 30, 2015
Citation: Alkhiary W, Abdalaal M, El-Sabbagh A (2015) Serum Concentrations of Interleukin-33 and its Soluble Receptor sST2 in Patients with Persistent Atrial Fibrillation. J Mol Biomark Diagn 6:235. doi:10.4172/2155-9929.1000235
Copyright: © 2015 Alkhiary W, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objectives: Interleukin-33 (IL-33) is a new member of the IL-1 cytokine family, which is thought to be involved in the pathogenesis of various inflammatory diseases, through its soluble receptor ST2. There is increasing evidence that inflammation is a relevant player in structural atrial remodeling that represents the main mechanism for atrial fibrillation (AF) persistence. This study was designed to investigate the state of IL-33/ST2 axis serum concentrations in patients with persistent AF.
Design and Methods: We investigated the concentrations of IL-33, its soluble ST2 receptors, and high-sensitivity C-reactive protein levels (hsCRP) in the sera of 92 patients with persistent atrial fibrillation, and 68 controls.
Results: Serum concentrations of IL-33, sST2, and hsCRP were all significantly elevated in patients with persistent AF compared to controls (P <0.0001 for all). Moreover, serum IL-33 concentrations was positively correlated with the inflammatory marker hsCRP (r=0.606, P =0.002).
Conclusion: These preliminary results may support the role of inflammation in AF pathogenesis and IL-33/sST2 axis may be involved in the inflammatory process in AF.