Increased serum interleukin‐32 levels in patients with Behçet's disease

Aim Interleukin (IL)‐32 is known to act as a proinflammatory cytokine and is likely involved in several chronic inflammatory diseases. The aims of this study were to investigate whether serum IL‐32 levels are elevated in patients with Behçet's disease (BD) and to identify the correlation betwee...

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Veröffentlicht in:International journal of rheumatic diseases 2018-12, Vol.21 (12), p.2167-2174
Hauptverfasser: Ha, You‐Jung, Park, Jin‐Su, Kang, Mi‐il, Lee, Soo‐Kon, Park, Yong‐Beom, Lee, Sang‐Won
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Sprache:eng
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Zusammenfassung:Aim Interleukin (IL)‐32 is known to act as a proinflammatory cytokine and is likely involved in several chronic inflammatory diseases. The aims of this study were to investigate whether serum IL‐32 levels are elevated in patients with Behçet's disease (BD) and to identify the correlation between IL‐32 levels and disease activity. Methods We enrolled 50 patients with BD and 35 healthy controls. Serum IL‐32 levels were measured using an enzyme‐linked immunosorbent assay. Serum levels of IL‐12p70, IL‐17A, IL‐1β, IL‐6 and IL‐8 were measured using a multiplex assay. BD disease activity was determined using the Behçet's Disease Current Activity Form (BDCAF). Results Serum IL‐32 levels were significantly higher in patients with BD (median [interquartile ranges], 0.4 [0.1–736.2] pg/mL) than in healthy controls (0.1 [0.1–14.7] pg/mL, P = 0.041). When patients with BD were divided into active (patient index score ≥ 2 or transformed index score ≥ 5 in the BDCAF) and inactive groups, IL‐32 levels tended to be higher in patients with active BD, although this observation was statistically insignificant. Serum levels of IL‐12p70, IL‐17A, IL‐1β, IL‐6 and IL‐8 did not differ between active and inactive groups. There was a weak positive correlation between serum IL‐32 levels and BDCAF scores (R = 0.301, P = 0.033). BD patients with recent arthralgia exhibited higher IL‐32 levels than did those without (P < 0.001). Conclusion These findings suggest that IL‐32 may play a minor role in the pathogenesis of BD.
ISSN:1756-1841
1756-185X
DOI:10.1111/1756-185X.13072