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SBE is not only easy to perform, due to the single balloon, but it can also safely examine the deep small intestine. Therefore, SBE may be a useful diagnostic and therapeutic tool in addition to DBE for investigating suspected small bowel disease.

IL-33, derived from colonic SEMFs, may play an important role in the pathophysiology of UC.

SummaryInterleukin (IL)-32 is a recently described proinflammatory cytokine, characterized by induction of nuclear factor (NF)-kB activation. We studied IL-32a expression in the inflamed mucosa of inflammatory bowel disease (IBD). We also investigated mechanisms regulating IL-32a expression. Tissue samples were obtained endoscopically or surgically from patients with ulcerative colitis (UC) (n = 10), Crohn's disease (CD) (n = 10), ischaemic colitis (n = 4) and normal colorectal tissues (n = 10). IL-32a expression was evaluated by standard immunohistochemical procedure. IL-32 mRNA expression was analysed by Northern blot. IL-32a was expressed weakly by colonic epithelial cells from normal individuals and subjects with ischaemic colitis. In the inflamed mucosa of IBD patients, epithelial IL-32a expression was increased markedly. In UC and CD patients, IL-32a expression was enhanced in affected mucosa compared to non-affected mucosa. In intestinal epithelial cell lines, expression of IL-32a mRNA and protein was enhanced by IL-1b, interferon (IFN)-g and tumour necrosis factor (TNF)-a. A combination of TNF-a plus IFN-g exerted synergistic effects. IL-32a induction by IL-1b and/or TNF-a was mediated by NF-kB activation. Epithelial IL-32a expression was increased in IBD patients, and in CD patients in particular. IL-32a might be involved in the pathophysiology of IBD as a proinflammatory cytokine and a mediator of innate immune response.