ArticleReumatologia
Cytokines and integrins related to inflammation of joint and gut in patients with spondyloarthritis and inflammatory bowel disease.
Article in Reumatologia. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Clinical Features and Outcomes of Coronavirus Disease 2019 in Patients with Inflammatory Bowel Disease and Spondyloarthropathies.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022Article
- Analyzing the Role of Gut Microbiota on the Onset of Autoimmune Diseases Using TNFMicroorganisms · 2021Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesInflammatory 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
methodsPatients with SpA (
resultsComparison 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 (
conclusionsPatients 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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