Oxidative stress and immunological biomarkers in Ankylosing spondylitis patients

Abstract

Ankylosing spondylitis (AS) is an inflammatory condition with unrevealed etiology mostly affecting the peripheral joints, the axial skeleton and extra articular structure. In recent years, oxidative stress and immunological factors have been reported as significant factors in AS pathogenesis. The object of this research was to assess the immunological and the oxidative stress factors in AS patients. In this study, 35 patients diagnosed with AS and 40 healthy controls were subjected for clinical examination. Patients were evaluated for Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). The biomarkers of oxidative stress were evaluated by biochemical assays. We evaluated the mRNA level of transcription factors, cytokines, chemokines and related miRNAs. T Helper 17 cells (Th17), regulatory T cells (Treg) proportion and cytokines secretion were also assessed. Higher levels of nitric oxide (NO) (p < 0.0001), superoxide dismutase (SOD) (p = 0.0002), total oxidant status (TOS) (p = 0.0041) and catalase (CAT) (p = 0.0002) were observed in AS patients. However, no significant differences in glutathione peroxidase (GPX) activity level were observed between studied groups. Also, in peripheral blood of AS patients, Th17 (p < 0.0001) and Treg (p = 0.0006) cells were significantly increased and decreased compared to the healthy controls. Nuclear factor (NF)-κB and Activation protein (AP)-1 mRNA expression levels were also increased in AS patients (p = 0.0001 and p = 0.0004, respectively). A significant decrease in miR-146a and miR-223 (p < 0.0001 and p = 0.0025, respectively) and increase in miR-21 (p = 0.0018) expression level were similarly observed in AS patients. Moreover, the secretion of tumor necrosis factor (TNF)-α (p < 0.0001), Interleukin (IL)-1β (p = 0.0002), CCL2 (p < 0.0001), CCL3 (p < 0.0001), CXCL8 (p = 0.0006) and adiponectin (p = 0.0002) were increased in AS patients. Our results showed that immunological and oxidative stress biomarkers play key roles in AS pathogenesis probably mediated by inflammation.