Author/Authors :
Eskandari Torbaghan، Yaser نويسنده 1Department of Immunology, International Campus, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. , , Kazemi Arababadi، Mohammad نويسنده 2Department of Laboratory Sciences, Faculty of Laboratory Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran , , Shams، Ali نويسنده 3Department of Immunology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. ,
Abstract :
Background and Aims: Engagement of the receptor for advanced glycation end products (RAGE) and its ligand “S100A12 protein” induce a cascade of reactions that eventually might lead to develop an inflammatory response dependent on NF-?B. Although involvement of S100A12 and RAGE in some autoimmune disease have proved, in chronic hepatitis B (CHB) infection functions of the proteins are not clear thus far. Determining of expression of S100A12 and RAGE in peripheral blood cells of the CHB patients was the aim of the present study.
Materials and Methods: In the case-control study the mRNA levels of S100A12 and RAGE genes of the sixty CHB patients and sixty healthy donors were measured by real-time polymerase chain reaction method. The patients and healthy donors were sex and age-matched.
Results: The findings demonstrated expression of S100A12 and RAGE in the CHB patients significantly decreased compared to the healthy donor group (p=0.001). Expression levels of the genes were not altered among HBeAg-positive and HBeAg-negative CHB patients. The HBV-DNA copy number/ml did not affect the expression of S100A12 and RAGE in the patients (p > 0.05).
Conclusions: The results of the study suggested that down regulation of RAGE and S100A12, because of their role in inducing inflammation, might have a considerable role in chronicity of hepatitis B.