P028 Inflammatory bowel disease is associated with cytoskeleton rearrangement in the epithelial cells
A. Portyanko1, P. Perevoschikov1, K. Ruksha1, J. Gorgun*2
1Belarusian State Medical University, Department of Pathology, Minsk, Belarus, 2Belarusian Medical Academy of Postgraduate Education, Department of Gastroenterology and Nutrition, Minsk, Belarus
It is known that the expression of beta-tubulin isotypes is changed in colorectal cancer, but there are still no data about such alterations in inflammatory bowel disease (IBD). Therefore, the aim of this study was to reveal any changes in the level of betaI-isotype of tubulin in IBD.
The study was performed on biopsy fragments of colonic mucosa from 61 patients: 12 with Crohn’s disease (CD), 27 with ulcerative colitis (UC), and 22 control persons with normal colonic mucosa. Double immunofluorescence with anti-cytokeratin antibody and anti-betaI-tubulin was performed. The level of the betaI-tubulin expression was analysed using eCognition software (Trimble, Germany): epithelial regions were automatically selected by cytokeratin channel; acquired regions of interest have been used as a mask of selection on tubulin channel; integrated density and area of regions of interest were measured. Expression value was calculated as ratio of integrated density to epithelial region’s area and then normalised according to positive and negative controls. On slides stained by haematoxylin and eosin, histological features were assessed including neutrophils in epithelium, crypt destruction, erosion,, and presence of dysplasia.
The expression of betaI-tubulin was detected in epithelial cells in both inflamed and normal colonic mucosa. In the joined IBD group, the level of betaI-tubulin was significantly reduced (p = 0.000). However, in the CD group, the expression was increased as compared with the both control (p = 0.029) and UC groups (p = 0.000). The linear regression revealed significant relation of betaI-tubulin with the presence of dysplasia (p = 0.000). No relation was found with disease activity signs, mucus depletion, and crypt depletion.
These results demonstrate for the first time that betaI-tubulin expression is altered in IBD, and this phenomenon has the opposite directions in CD and UC. Further investigations are needed to understand the clinical significance of these findings.