Ahmed Abdul-Hassan Abbas, Raghad Raad Hwyidii and Khalid A. AL-Khazraji
Keywords: IBD, IL-33, soluble ST2, ulcerative colitis.
Abstract: The etiopathogenic hypothesis for inflammatory bowel disease (IBD) suggests an immune mediated process originates from an inappropriate response of immune system. This study was performed to evaluate the role of IL-33 and sST2 in pathogenesis of IBD and to correlate their levels with the disease activity and with serum levels of p-ANCA and ASCA. Fifty five patients with IBD (41 UC patients and 14 CD patients) and 25 subjects as controls were participated in this study. Blood samples were collected from all patients and controls to assess serum concentrations of IL-33, sST2, p- ANCA and ASCA by enzyme-linked immune-sorbent assay. There was significant elevation in serum level of IL-33 among UC and CD patients as compared to controls, where a serum level of sST2 was increase significantly only in UC patients when compared to controls. In addition the serum level of IL-33 was lower in treated patients with infliximab than patients on other treatments but statistically not significant. While the comparison between patients who receive infliximab versus patients with other treatment revealed significant differences in serum level of sST2. High positively of p-ANCA in UC patients and ASCA in CD patients were found as compared with control. Another important result in UC patients there was positive correlation between serum IL-33 and sST2 and the disease activity, also IL-33 level was positively correlated with each of sST2 and p-ANCA. IL-33 and sST2 might be a crucial mediator in pathogenesis of IBD. In addition, the increased levels of IL33 and sST2 correlated with disease activity of UC possibly reflect an acute response due to inflammation. Also, in particular, IL-33 may regulate by TNF-? in UC.
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