Autoantibody against peroxiredoxin I, an antioxidant enzyme, in patients with systemic sclerosis: possible association with oxidative stress.
ABSTRACT To determine the prevalence and clinical correlation of autoantibody to peroxiredoxin (Prx) I, an antioxidant enzyme, in patients with systemic sclerosis (SSc).
Serum samples from SSc patients (n = 70) and healthy controls (n = 23) were examined by ELISA using human recombinant Prx I. The presence of anti-Prx I antibody was further evaluated by immunoblotting analysis. To determine the functional relevance of anti-Prx I antibody in vivo, we assessed whether anti-Prx I antibody was able to inhibit Prx I enzymatic activity using yeast thioredoxin reductase system.
IgG anti-Prx I antibody levels in SSc patients were significantly higher than healthy controls and this autoantibody was detected in 33% of SSc patients. The presence of IgG anti-Prx I antibody was associated with longer disease duration, more frequent presence of pulmonary fibrosis, heart involvement, and anti-topoisomerase I antibody and increased levels of serum immunoglobulin and erythrocyte sedimentation rates. IgG anti-Prx I antibody levels also correlated positively with renal vascular damage and negatively with pulmonary function tests. Furthermore, anti-Prx I antibody levels correlated positively with serum levels of 8-isoprostane, a marker of oxidative stress. Immunoblotting analysis confirmed the presence of anti-Prx I antibody. Remarkably, Prx I enzymatic activity was inhibited by IgG isolated from SSc sera containing IgG anti-Prx I antibody.
These results suggest that elevated IgG anti-Prx I autoantibody is associated with the disease severity of SSc and that anti-PrxI antibody may enhance the oxidative stress by inhibiting Prx I enzymatic activity.
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ABSTRACT: Abstract Context: Systemic sclerosis (SSc) is an autoimmune disease with incompletely known physiopathology. There is a great challenge to predict its course and therapeutic response using biomarkers. Objective: To critically review proteomic biomarkers discovered from biological specimens from systemic sclerosis patients using mass spectrometry technologies. Methods: Medline and Embase databases were searched in February 2014. Results: Out of the 199 records retrieved, a total of 20 records were included, identifying 116 candidate proteomic biomarkers. Conclusion: Research in SSc proteomic biomarkers should focus on biomarker validation, as there are valuable mass-spectrometry proteomics studies in the literature.Biomarkers 05/2014; · 1.88 Impact Factor
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ABSTRACT: Introduction: Coeliac Disease (CD) is an immune-mediated chronic inflammatory disease of upper small intestine in genetically permanent gluten-sensitive individuals. Oxidative stress was reported to play an important role in the pathogenesis of coeliac disease. The aim of this study was to investigate the frequency of the polimorphisms in the structures of the enzymes SOD and GSHPx with changing levels depending on increased oxidative stress and whether there is an association with the mutations DQA1*0501, DQB1*0201, DRB1*04 reported frequently in coeliac disease. Methods: This study has investigated SOD and GSH-PX polymorphisms and the frequently reported mutations DQA1*0501, DQB1*0201 and DRB1*04 in the patients with CD. Height and weight measurements of the patients were obtained to evaluate their growth and development, also correlation between polymorphisms SOD and GSH-PX and concerned mutations were investigated. Results: This study involved total 56 cases, 35 female (62.5%) and 21 male (37.5%), with a mean age 6.66 ± 4.18 years. Polymorphisms SOD and GSH-PX were found in homozygote, heterozygote and wild-type patients. At least one of the mutations DQA1*0501, DQB1*0201 and DRB1*04 were found in 41 patients. Conclusion: Although etiology of coeliac disease is not entirely clear, many mechanisms have been suggested. It may be observed that the retardation of growth and development in the patients with coeliac disease may be associated with oxidative stress and decreased antioxidant capacity.Healthmed 01/2011; 5(5):1008-1013. · 0.44 Impact Factor