Abstract
BackgroundThe role of IL-12/23 in the pathogenesis of ulcerative colitis (UC) is unclear. We analyzed mucosal IL-12/23 expression and its relationship with endoscopic severity, histological activity, and UC relapse.MethodsRectal biopsies were collected from 70 UC patients with clinical remission. IL-12, IL-23, IFN-γ, IL-17A, and IL-17F mRNA expression was measured by real-time PCR. Endoscopic severity and histological activity were evaluated using the Mayo endoscopic subscore (MES) and the Geboes score, respectively.ResultsThe longest follow-up period was 51 months. Thirty-four patients relapsed during the study period. Samples from these subsequently relapsed patients formed the “relapse” group, while those from patients that did not relapse formed the “remission” group. IL-12 (P = 0.0003) and IL-23 (P = 0.014) mRNA expression was significantly higher in the relapse than the remission group. Expression of IL-23 (P = 0.015) but not IL-12 (P = 0.374) was correlated with MES. However, in patients with an MES of 0 and 1, IL-12 expression was statistically higher in the relapse than the remission group (P = 0.0015, P = 0.0342). IL-12 and IL-23 expression did not vary significantly between histologically active and inactive mucosa; both were higher in histologically inactive patients in the remission group (IL-12: P = 0.0002, IL-23: P = 0.046).ConclusionsRectal IL-12 and IL-23 expression was elevated in the relapse group, but IL-12 was more strongly associated with UC relapse, irrespective of endoscopic severity and histological activity. Mucosal IL-12 was elevated in patients with deep mucosal healing. Our results suggest an important role of IL-12 in UC pathogenesis and the molecular mechanism of UC relapse.
Highlights
The role of IL-12/23 in the pathogenesis of ulcerative colitis (UC) is unclear
In conclusion, upregulation of IL-12 in the rectal mucosa of patients with UC in clinical remission was associated with relapse
IL-12 upregulation is independent of both endoscopic severity and histological activity with regard to UC relapse
Summary
The role of IL-12/23 in the pathogenesis of ulcerative colitis (UC) is unclear. Inflammatory bowel diseases (IBD), which include ulcerative colitis (UC) and Crohn’s disease (CD), are chronic conditions characterized by recurrent intestinal inflammation. A complex network of immune cells, such as. T-helper cells, and cytokines such as interleukins, are involved in the pathogenesis of IBD. Since inflammatory mediators have been implicated in the pathogenesis of IBD, these molecules have been utilized as therapeutic targets for its treatment. TNF-α was the first molecule to be identified as a therapeutic target to control IBD [1]. Many TNF-α inhibitors have been clinically approved for treatment of CD and UC. Other cytokines have been targeted to developed new therapeutics and have been
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