Abstract
AbstractAim: More and more studies have demonstrated that the interleukin (IL)-23/IL-17 axis is highly associated with immune dysfunction and activated autoimmune inflammation. The purposes of this study were to determine the serum levels of IL-17 and IL-23 in ankylosing spondylitis (AS) patients compared with healthy controls and evaluate these cytokine levels based on disease-related characteristics. Material and Methods: Eighty-six consecutive AS patients and 70 sex and age-matched healthy controls were included in the study. The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), the Ankylosing Spondylitis Disease Activity Score (ASDAS)-erythrocyte sedimentation rate (ESR), ASDAS-C reactive protein, the Bath Ankylosing Spondylitis Functional Index (BASFI), the Spondyloarthritis Research Consortium of Canada (SPARCC) enthesitis index, the Bath Ankylosing Spondylitis Metrology Index (BASMI), the Ankylosing Spondylitis Quality of Life Questionnaire (ASQoL) and Achilles pain VAS scores were recorded. Serum IL-17 and IL-23 levels were examined by enzyme-linked immunosorbent assay. Results: The serum levels of IL-17, IL-23 and CRP as well as ESR values were significantly increased in AS patients compared with controls (1.94 vs. 0.28 pg/mL p ˂ 0.001; 82.9 vs. 44.3 pg/mL p ˂ 0.001; 0.48 vs. 0.30 mg/dL, p=0.001; 12±13.9 vs. 8±6.8 mm/h, p=0.003, respectively). In AS patients, serum IL-17 levels were significantly correlated with the ASDAS-ESR and ASDAS-CRP (r=0.244, p=0.024; r=0.258, p=0.017), but not with ESR, CRP, BASDAI, function, mobility, quality of life, enthesitis index or Achilles pain scores (all p>0.05). Serum IL-23 levels demonstrated a significant correlation with Achilles pain VAS, but not with other disease-related parameters (all p>0.05). Conclusions: AS patients had increased serum IL-17 and IL-23 levels compared with healthy controls, and serum IL-17 levels were associated with disease activity. Our study results support the hypothesis that the IL17/23 pathway plays an important role in the pathogenesis of AS.
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