Umeå universitets logga

Background: Macrophage migration inhibitory factor (MIF) is a multipotent cytokine involved in the regulation of immune and inflammatory responses. The present study aimed to investigate the MIF expression in patients with ankylosing spondylitis (AS) compared with controls and to examine associations between MIF and demographic and inflammation related factors in AS overall and stratified by sex.

Methods: MIF in plasma was measured in a cohort of patients with AS from Northern Sweden (n= 155) and age- & sex-matched controls (n=151) using Human MIF Quantikine ELISA Kit (R&D). The patients were assessed with laboratory markers of inflammation, ASDAS-CRP, BASDAI, BASMI and BASFI. Comparisons were analyzed by T-test and associations by bivariate Pearson correlations.

Results: The expression of MIF was significantly augmented in the AS patients (Mean 65.1 ng/ml±2.0 SEM) compared with the controls (Mean 42.0 ng/ml±2.1 SEM) (p<0.001), the difference was also found in sex stratified analyses. MIF had a weak negative correlation with age in AS (-0.144, p=0.07) but not in controls (-0.037, p=0.66). Stratified by sex, the inverse correlation with age was shown in the AS men only (-0.28, p=0.004). When analyzing MIF in different age-groups it was revealed that MIF was significantly higher in the men ≤50 years compared to the women with AS ≤50 years. Moreover, MIF was positively correlated with inflammation related variables; swollen joint count, ESR, hsCRP, thrombocytes and leukocytes. The expression of MIF was significantly increased in AS patients on cDMARDs with or without a biological drug, while NSAIDs, glucocorticosteriods or single therapy with a biological drug did not influence the MIF levels.

Conclusions: Our results suggest that MIF is overexpressed in AS patients. MIF was associated with inflammation and treatment and, in addition, sex seemed to have an impact on MIF plasma levels in the AS patients. MIF might be a potential biomarker for the development of new treatment-strategies in AS.