Abstract
Interleukin (IL)-17 and IL-23 are crucial for mediating gut mucosal inflammation in inflammatory bowel disease (IBD), which has led to new therapeutic strategies. We assessed the relevancy of IL-17 and IL-23 serum levels as potential biomarkers towards severe IBD discrimination and disease-related complications. Sixty-two patients diagnosed with Crohn’s disease (CD) and ulcerative colitis (UC) were included. Serum IL-17 and IL-23 were measured by sandwich enzyme-linked immunosorbent assays (ELISA). IL-23 and fecal calprotectin (FCal) were significantly higher in severe CD (p < 0.001) and UC (p < 0.001 and p = 0.001, respectively), compared to mild or moderate. Elevated C-reactive protein (CRP) was correlated with severe disease only in CD (p = 0.008), whereas for UC, disease severity was associated with increased IL-17 values (p < 0.001). Diagnostic role of IL-23 was superior to FCal in discriminating between severe and mild to moderate CD (p < 0.001). IL-23 levels were also significantly higher in CD patients with intestinal complications (p = 0.04). Both IL-17 and IL-23 correlate with IBD severity, and IL-23 might be a promising novel biomarker for severe CD. Identifying the dominant IL pathway involved in IBD severity could serve as guidance for clinical decision-making on biologic therapy.
Highlights
Identifying the dominant IL pathway involved in inflammatory bowel disease (IBD) severity could serve as guidance for clinical decision-making on biologic therapy
Based on the criteria described in the method section (Table S1), 16 patients with Crohn’s disease (CD) and ulcerative colitis (UC) patients were classified as having mild-to-moderate disease, whereas CD and 17 UC patients were included in the severe disease group
We have shown that serum levels of IL-17 and IL-23 could become a valuable biomarker for assessing disease severity subtypes in both CD and UC, by testing these molecules against biomarkers frequently used in clinical practice such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), albumin, and
Summary
Ulcerative colitis (UC) and Crohn’s disease (CD) are chronic disorders of the gastrointestinal tract with a complex etiology that involves immune, genetic, and environmental factors. Disease progression and severity are highly variable across individuals with inflammatory bowel disease (IBD), which suggests that distinct cytokine pathways may be responsible for the heterogeneity of clinical outcomes [1]. Interleukin (IL)-23/T helper (Th)-17 cytokine pathway was found to have a key role in driving gut inflammation and the development of several other chronic inflammatory diseases, such as psoriasis, rheumatoid arthritis, and multiple sclerosis [2]. Genome-wide association studies have linked IL-23 to IBD susceptibility via polymorphisms in the IL-23 receptor (IL-23-R) gene that enhances the activity of the IL-17/IL-23 pathway [3]
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