Evaluation of interleukins (IL-1α, IL-1Ra, IL-12, IL-17A, IL-31, and IL-33) and chemokines (CXCL10 and CXCL16) in the serum of male patients with ankylosing spondylitis

• Published in: International immunopharmacology 2024-03, Vol.129, p.111697-111697, Article 111697
• Main Authors: Muhsin, Hanan Y., Khazaal, Ali Q., Ismaeel, Haneen M., Alosami, Mohammed H., Ad'hiah, Ali H.
• Format: Article
• Language: English
• Subjects: Ankylosing spondylitis; Area under the curve; Case-Control Studies; Chemokine; Chemokine CXCL10; Chemokine CXCL16; Cytokines; Humans; Interleukin; Interleukin 1 Receptor Antagonist Protein; Interleukin-12; Interleukin-17; Interleukin-1alpha; Interleukin-33; Interleukins; Male; Odds ratio; Spondylitis, Ankylosing - diagnosis
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2024.111697

•Serum levels of IL-17A, CXCL10, and CXCL16 were up-regulated in male patients with ankylosing spondylitis.•Serum IL-31 levels were down-regulated in in male patients with ankylosing spondylitis.•IL-17A, IL-31, CXCL10, and CXCL16 were potential markers to differentiate between ankylosing spondylitis patients and controls.•IL-1α, IL-1Ra, IL-12, and IL-33 levels showed no significant variations between ankylosing spondylitis patients and controls. A case-control study was performed to explore eight pro-inflammatory and anti-inflammatory cytokines, namely interleukin (IL)-1α, IL-1Ra (IL-1 receptor antagonist), IL-12, IL-17A, IL-31, IL-33, CXCL10 (C-X-C motif chemokine ligand 10), and CXCL16, with the aim to understand their role in ankylosing spondylitis (AS) pathogenesis and evaluate their utility as markers to differentiate between diseased and healthy individuals. Among these cytokines, IL-31 and CXCL16 have not been well studied in AS. The study included 94 male patients with AS and 91 age-matched control males. Interleukin and chemokine levels were measured using ELISA kits. Serum levels of IL-17A, CXCL10, and CXCL16 were significantly elevated in patients compared to controls, while IL-31 levels were significantly decreased in patients. IL-17A, CXCL10, and CXCL16 were associated with an increased risk of AS, while IL-31 was associated with a decreased risk of disease (odds ratio = 1.22, 1.78, 1.14, and 0.89, respectively). As indicated by the area under the curve (AUC), IL-17A, IL-31, CXCL10, and CXCL16 were potential markers to differentiate between AS patients and controls (AUC = 0.877, 0.735, 0.8, and 0.7, respectively). IL-1α, IL-1Ra, IL-12, and IL-33 levels showed no significant variations between patients and controls. Among the eight cytokines examined, IL-17A, CXCL10, and CXCL16 were up-regulated in the serum of AS patients, while IL-31 was down-regulated. The levels of IL-1α, IL-1Ra, IL-12, and IL-33 showed no significant differences between patients and controls. Serum levels of all cytokines were not affected by disease duration, HLA-B27 positivity, or disease activity.