Malarial Infection of Female BWF1 Lupus Mice Alters the Redox State in Kidney and Liver Tissues and Confers Protection against Lupus Nephritis

被引:10
作者
Al-Quraishy, Saleh [1 ]
Abdel-Maksoud, Mostafa A. [1 ,2 ]
El-Amir, Azza [1 ]
Abdel-Ghaffar, Fathy A. [2 ]
Badr, Gamal [3 ]
机构
[1] King Saud Univ, Coll Sci, Dept Zool, Riyadh 11451, Saudi Arabia
[2] Cairo Univ, Fac Sci, Dept Zool, Cairo 61616, Egypt
[3] Assiut Univ, Lab Immunol & Mol Biol, Dept Zool, Fac Sci, Assiut 71516, Egypt
关键词
TUMOR-NECROSIS-FACTOR; LIPID-PEROXIDATION; AUTOIMMUNE-DISEASE; ERYTHEMATOSUS; GLUTATHIONE; APOPTOSIS; TNF; ANTIBODIES; PROTEIN; IL-10;
D O I
10.1155/2013/156562
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
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页数:10
相关论文
共 41 条
[1]   Low frequency of autoimmune disease in tropical Africa [J].
Adebajo, AO .
LANCET, 1997, 349 (9048) :361-362
[2]  
Aebi H, 1984, METHODS ENZYMATIC AN
[3]   Oxygen free radicals and systemic autoimmunity [J].
Ahsan, H ;
Ali, A ;
Ali, R .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2003, 131 (03) :398-404
[4]  
Amital H., 2004, SYSTEMIC LUPUS ERYTH, P3
[5]   Circulating plasma levels of nucleosomes in patients with systemic lupus erythematosus - Correlation with serum antinucleosome antibody titers and absence of clear association with disease activity [J].
Amoura, Z ;
Piette, JC ;
Chabre, H ;
Cacoub, P ;
Papo, T ;
Wechsler, B ;
Bach, JF ;
Koutouzov, S .
ARTHRITIS AND RHEUMATISM, 1997, 40 (12) :2217-2225
[6]  
[Anonymous], 1959, ARCH BIOCHEM BIOPHYS
[7]   Tumour necrosis factor and other proinflammatory cytokines in systemic lupus erythematosus: a rationale for therapeutic intervention [J].
Aringer, M ;
Smolen, J .
LUPUS, 2004, 13 (05) :344-347
[8]   Increased bioactive TNF in human systemic lupus erythematosus:: associations with cell death [J].
Aringer, M ;
Feierl, E ;
Steiner, G ;
Stummvoll, GH ;
Höfler, E ;
Steiner, CW ;
Radda, I ;
Smolen, JS ;
Graninger, WB .
LUPUS, 2002, 11 (02) :102-108
[9]   The role of tumor necrosis factor-alpha in systemic lupus erythematosus [J].
Aringer, Martin ;
Smolen, Josef S. .
ARTHRITIS RESEARCH & THERAPY, 2008, 10 (01)
[10]  
Berkels Reinhard, 2004, V279, P1