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-α in UC.
Keywords: IBD, IL-33, soluble ST2, ulcerative colitis.
(FULL ARTICLE LINK) Read more ...
Vol. 9, No. 3, pp. 3541-3547, October 2015
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