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P076. Epithelial apoptotic loss is enhanced even in tissue from uninflamed mucosa in patients with Crohn's disease

P. Eder1, L. Lykowska-Szuber1, I. Krela-Kazmierczak1, K. Stawczyk-Eder1, K. Iwanik2, M. Zabel3, K. Linke1, 1Poznan University of Medical Sciences, Department of Gastroenterology, Human Nutrition and Internal Diseases, Poznan, Poland, 2Poznan University of Medical Sciences, Department of Clinical Pathomorphology, Poznan, Poland, 3Poznan University of Medical Sciences, Department of Histology and Embryology, Poznan, Poland

Background

Enhanced apoptosis seems to play an important role in the pathogenesis of epithelial barrier dysfunction in patients with Crohn's disease (CD), however the direct mechanisms of these phenomena are poorly understood. The aim of this study was to assess the expression of proteins related to apoptosis in colonic epithelium in both inflamed and uninflamed mucosa and to compare it with healthy conditions.

Methods

Patients with active CD were qualified for the study. Each patient underwent colonoscopy with the assessment of endoscopic activity of CD. Biopsies from inflamed and uninflamed areas of the colon were obtained. Clinical and biochemical data were also collected. Expression of an active caspase 3, Bax, Bcl-2, Fas and TNFR1 proteins were assessed in colonic epithelium by using immunocytochemical methods. Colonic biopsies taken from a healthy gut were used as a control tissue.

Results

50 patients were qualified for the study. The expression of an active caspase 3 was significantly higher in inflamed colonic tissue from patients with CD when compared with uninflamed mucosa and with the control group. However the expression of an active caspase 3 was also significantly stronger in epithelial cells from uninflamed mucosa when compared with the healthy gut. There were no differences in the Bax/Bcl-2 ratios between the study groups. The expression of Fas and TNFR1 was significantly higher in inflamed mucosa, when compared with uninflamed intestinal tissue and with the healthy gut. The expression of TNFR1 was also significantly higher in uninflamed intestinal CD tissue comparing with the control group. There was a significant correlation between TNFR1 and active caspase 3 expression in inflamed colonic epithelium in CD patients.

Conclusion

Epithelial apoptotic loss was enhanced not only in inflamed mucosa in patients with CD, but also in epithelium from uninflamed CD tissue when compared with the healthy gut. These phenomena were related to the extrinsic apoptotic pathway. Our study shows that even in macroscopically normal gut there is a defect of epithelial cells function in patients with CD in comparison with physiological conditions.