Abstract

Neuropsychiatric Systemic Lupus Erythematosus (NPSLE) has multiple pathogenic mechanisms that cause diverse manifestations and whose diagnosis is challenging because of the absence of appropriate diagnostic tests. In the present study the application of proteomics using two-dimensional electrophoresis (2D) and mass spectrometry (MS) allowed the comparison of the protein profile of the serum low and high abundance protein fractions of NPSLE patients (NPSLE group) and SLE without neuropsychiatric syndromes (SLE group), Neuropsychiatric syndromes not associated with SLE (NPnoSLE groups), and healthy controls (CTRL group). The gels obtained were digitalized and analyzed with the PDQuest software. The statistical analysis of the spots was performed using the nonparametric Kruskal Wallis and Dunn's multiple comparison tests. Two spots showed significant differences and were identified by MS. Spot 4009 was significantly lower in NPSLE with regard to NPnoSLE (p= 0,004) and was identified as apolipoprotein A1 (APOA1) (score 809-1132). Spot 8001 was significantly higher in NPSLE regarding CTRL and NPnoSLE (p= 0,01 y 0,03, respectively) and was identified as serum amyloid A (SAA) (score 725-2488). The proinflammatory high density lipoproteins (HDL) have been described in SLE. In this HDL the decrease of APOA1 is followed by an increase in SAA. This altered level of both proteins may be related to the inflammatory state that is characteristic of an autoimmune disease like SLE, but this is not specific for NPSLE.

Highlights

  • Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease caused by the loss of immune tolerance to nuclear and cytoplasmic autoantigens in genetically susceptible individuals exposed to environmental triggers

  • Neuropsychiatric Systemic Lupus Erythematosus (NPSLE) comprises 19 syndromes described by the American College of Rheumatology (ACR) [3]

  • The decrease in apolipoprotein A1 (APOA1) and the increase in serum amyloid A (SAA) showed in NPSLE in this study may be related to the inflammatory state that is characteristic of an autoimmune disease like SLE

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Summary

Introduction

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease caused by the loss of immune tolerance to nuclear and cytoplasmic autoantigens in genetically susceptible individuals exposed to environmental triggers. There is a failure in the Autoimmune Diseases attribution of neuropsychiatric symptoms to SLE (known as primary NPSLE) or as a result of nervous system injuries indirectly involved with SLE (secondary NPSLE) [6]. This makes the correct attribution of neuropsychiatric syndromes to SLE dependent on an exclusion process, because of the absence of a diagnostic gold standard useful for these manifestations [7]

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