Background Ankylosing spondylitis (AS) is a clinically well-known chronic inflammatory disease of the axial skeleton and peripheral joints. The pathogenesis of this disease still remains a challenge. Determination of cytokine profile and its role involved in AS pathogenesis give an opportunity to extend the targeted therapeutic approach. Interleukin-17 (IL-17) and interleukin-23 (IL-23) are cytokines of interest in the investigation of the pathogenesis of spondyloarthritides although their importance in AS is not clearly defined.
Objectives to investigate levels of IL-17 and IL-23 in a group of AS and in a demographically matched group of healthy subjects and its association with the disease activity measured by relevant clinical and biochemical parameters.
Materials and Methods 39 AS patients classified by the modified New York and ASAS criteria were assessed clinically and 6 ml of serum were collected from each patient. 39 healthy subjects as control group were included in this study. The serum IL-17 and IL-23 levels were tested using xMAP multiplex immunobead assay technology. At the same time the disease activity was measured by using Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Ankylosing Spondylitis Disease Activity Score (ASDAS) using C-reactive protein (CRP), erythrocyte sedimentation rate (ESR).
Results The mean serum IL-17 and IL-23 level in AS group was respectively 18.9 (SD 39.6) and 194.6 (SD 261.4) pg/ml. In the healthy control group the mean serum IL-17 level was 15.4 (SD 26.0) and IL-23 level – 200.3 (SD 256.3) pg/ml. The serum levels of IL-17 and IL-23 were not statistically significantly different from the healthy subjects and the levels did not correlate with the disease activity measured by BASDAI and ASDAS (using the CRP and ESR).
Conclusions These results suggest that IL-17 and IL-23 are not major components of the pathogenesis of inflammation in AS patients. Our data differ from Chen W S et al, in 2012 published data of the serum IL-17 and IL-23 level association with the disease activity in Chinese patients with AS. This difference is probably due to the various genetic aspects characterising AS as geographically matched disease.
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