Cytokines and integrins related to inflammation of joint and gut in patients with spondyloarthritis and inflammatory bowel disease
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Submission date: 2017-10-03
Final revision date: 2017-11-23
Acceptance date: 2017-11-28
Online publication date: 2017-12-30
Publication date: 2017-12-31
Reumatologia 2017;55(6):276-283
Objectives: Inflammatory bowel disease (IBD) and spondyloarthritis (SpA) have some overlapping clinical features, i.e. gut and joint inflammation. Cytokines of interleukin 17(IL-17)/IL-23 axis play a pathogenic role in both diseases. Integrins (ITGs) regulate migration of immune cells to inflamed tissues (ITGβ7 into gut, ITGβ2 into gut and also to other tissues). In this study, we search for differences in the serum concentrations of these cytokines and integrins between patients suffering from SpA or IBD with and without overlapping symptoms.
Material and methods: Patients with SpA (n = 30), IBD (n = 68), and healthy volunteers (n = 28) were included in the study. Fourteen SpA patients reported symptoms characteristic for IBD. Spondyloarthritis symptoms were diagnosed in 50% of IBD patients, while other patients of this group reported arthralgia only. Serum concentrations of IL-17, IL-22, IL-23, ITGβ2, and ITGβ7 were measured by specific enzyme-linked immunosorbent assay using commercially available sets. The Mann-Whitney and Spearman’s rank tests were used for intergroup comparison and correlation assessment, respectively.
Results: Comparison of patient groups showed significantly higher serum concentrations of IL-17, IL-22, and ITGβ7 in SpA, and up-regulated levels of IL-23 in IBD patients. Similar differences were observed between patient subgroups, both with and without overlapping symptoms. In SpA but not in IBD patients, serum concentrations of ITGβ7 inversely correlated (r = –0.552) with C-reactive protein.
Conclusions: Patients with SpA and IBD differ in the circulating concentrations of IL-17/IL-23 axis cytokines and ITGβ7, irrespectively of the presence or absence of overlapping symptoms. Therefore, we conclude that observed differences are attributed rather to underlying than concurrent disease.
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