Depression and its related parameters increased the production of autoantibodies against 16α-hydroxyestrone-albumin complex in systemic lupus erythematosus.

Int Immunopharmacol

Department of Clinical Laboratory Science, College of Applied Medical Science, University of Hail, Hail 2440, Saudi Arabia; Molecular Diagnostic and Personalised Therapeutics Unit, University of Hail, Hail 2440, Saudi Arabia.

Published: June 2019

Depression is the common and early symptoms associated with early onset of SLE, 16α-hydroxyestrone (16α-OHE) levels were found to be significantly higher in serum and urine in patients with SLE. This study was carried out in order to know whether depression and its related parameters in the SLE patients enhanced the production of autoantibodies against 16α-OHE-albumin (A) complexes. The autoantibodies in the serum of 100 SLE [including 65 depressed SLE (DSLE)] patients and 37 control subjects were detected by using direct binding, inhibition ELISA and quantitative precipitin titration. Autoantibodies from DSLE patients (and also the patients who were taken anti-depressant and with neurological symptoms) showed high binding to 16α-OHE-A in contrast to SLE (p < 0.05) and control subjects (p < 0.001). Although, SLE sera showed high recognition to 16α-OHE-A in comparison to A (p < 0.05) or 16α-OHE (p < 0.001). The affinity of autoantibodies for 16α-OHE-A was found to be high for DSLE (1.16 × 10 M) and SLE (1.24 × 10 M) patients as detected by Langmuir plot. The concentration of 16α-OHE (p < 0.05) and inflammatory cytokines (IL-6, p < 0.05 and IL-17, p < 0.001) in the serum of SLE patients was found to be significantly higher than controls. Depression and its related parameters in SLE enhanced the production of autoantibodies against 16α-OHE-A through the generation of inflammatory conditions. Depression in SLE patients increased the release of pro-inflammatory cytokine (IL-6 and IL-17) that in turn generating more autoantibodies and showed strong recognition to 16α-OHE-A.

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http://dx.doi.org/10.1016/j.intimp.2019.03.036DOI Listing

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