%0 Journal Article
%T Malarial Infection of Female BWF1 Lupus Mice Alters the Redox State in Kidney and Liver Tissues and Confers Protection against Lupus Nephritis
%A Saleh Al-Quraishy
%A Mostafa A. Abdel-Maksoud
%A Azza El-Amir
%A Fathy A. Abdel-Ghaffar
%A Gamal Badr
%J Oxidative Medicine and Cellular Longevity
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/156562
%X Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by an imbalanced redox state and increased apoptosis. Tropical infections, particularly malaria, may confer protection against SLE. Oxidative stress is a hallmark of SLE. We have measured changes in the levels of nitric oxide (NO), hydrogen peroxide (H2O2), malondialdehyde (MDA), and reduced glutathione (GSH) in both kidney and liver tissues of female BWF1 lupus mice, an experimental model of SLE, after infection with either live or gamma-irradiated malaria. We observed a decrease in NO, H2O2, and MDA levels in kidney tissues after infection of lupus mice with live malaria. Similarly, the levels of NO and H2O2 were significantly decreased in the liver tissues of lupus mice after infection with live malaria. Conversely, GSH levels were obviously increased in both kidney and liver tissues after infection of lupus mice with either live or gamma-irradiated malaria. Liver and kidney functions were significantly altered after infection of lupus mice with live malaria. We further investigated the ultrastructural changes and detected the number of apoptotic cells in kidney and liver tissues in situ by electron microscopy and TUNEL assays. Our data reveal that infection of lupus mice with malaria confers protection against lupus nephritis. 1. Introduction Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease that is characterized by the appearance of autoantibodies, particularly against nuclear components [1]. Because of its multifactorial etiology, which includes genetic, hormonal, and environmental triggers, the molecular mechanisms underlying this disease remain largely unknown. Free-radical-mediated reactions have recently drawn considerable attention as a potential mechanism of the pathogenesis of SLE [2]. Excessive generation of reactive oxygen species (ROS) has the potential to initiate damage to lipids, proteins, and DNA [3]. ROS represent a part of the defense mechanisms against microbes in the body. In addition, increased ROS generation has been reported to promote inflammation, necrosis, and apoptosis in chronic kidney disease [4]. Furthermore, previous studies have reported an association between oxidative stress and autoimmunity in an autoimmune-prone MRL+/+ mouse model [5]. Indeed, apoptosis plays an important role in SLE, and higher apoptosis rates lead to the production of autoantibodies, subsequently triggering disease activity [6]. The percentage of apoptotic cells in peripheral blood is significantly higher in SLE patients than in normal
%U http://www.hindawi.com/journals/omcl/2013/156562/