This article aims to review recent literature linking epithelial barrier inflammation and arthritis in spondyloarthritis (SpA), with a critical view on how they are bound by genetic, immunological and environmental ties.
The epithelia-joint axis has become an intense area of both basic and clinical SpA research. The penultimate goal is to understand the immunopathologic links between epithelial inflammation and arthritis in SpA. Inflammatory bowel disease (IBD) and psoriasis (PsO) have strong links to SpA at several levels. Clinically, there is a strong association of IBD, PsO and SpA. Genetically, there are many shared risk factors; however, there are also distinct differences in the genetics of the respective diseases. Immunologically, type 3 immunity, especially interleukin (IL)-17 and IL-23 dysregulation, has been shown to play a central role in IBD, PsO and SpA. Environmentally, a microbial dysbiosis has been noted in each of these diseases, but whether the microbial signature is similar between diseases is not clear, nor is the effect of dysbiosis on the immune response known.
It will be crucial to determine whether the relationship between epithelia inflammation and SpA is truly causal for both the understanding of pathogenesis and for future treatment strategies.
aUnit Molecular Immunology and Inflammation, Inflammation Research Institute VIB-Ghent University
bDepartment of Rheumatology, Universitair Ziekenhuis Gent, University of Gent, Ghent, Belgium
cKrembil Research Institute, University Health Network
dDepartments of Immunology and Medicine, University of Toronto, Ontario, Canada
Correspondence to Eric Gracey, MRB 2, Corneel Heymanslaan 10, Ghent University Hospital Campus, Ghent 9000, Belgium. Tel: +32 093326842; fax: +32 093326842; e-mail: email@example.com