Histological analysis of ulcerative colitis using human pathology samples and mice deficient in sulfotransferases

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08343
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Human pathology
• Research Institution: University of Fukui
• Principal Investigator: KOBAYASHI Motohiro 福井大学, 学術研究院医学系部門, 教授 (00362137)
• Co-Investigator(Kenkyū-buntansha): 川島 博人 千葉大学, 大学院薬学研究院, 教授 (50260336)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 炎症性腸疾患 / 硫酸転移酵素 / 硫酸化糖鎖

Outline of Final Research Achievements

Mononuclear cell infiltrates in ulcerative colitis (UC) mucosa are considered to be recruited via high endothelial venule (HEV)-like vessels displaying mucosal addressin cell adhesion molecules 1 (MAdCAM-1), the ligand for integrin, and/or peripheral lymph node addressin (PNAd), an L-selectin ligand. 6-O-sulfation of N-acetylglucosamine in PNAd is catalyzed by N-acetylglucosamine-6-O-sulfotransferase 1 (GlcNAc6ST-1) and GlcNAc6ST-2. To determine the role of 6-O-sulfation on HEV-like vessels in UC, we employed a colitis model using mice deficient in both sulfotransferases (DKO mice). We found that more inflammatory cells were infiltrated in DKO mouse colitis, and the number of MAdCAM-1-positive vessels was increased in DKO mouse colitis. These findings suggest that MAdCAM-1 compensates PNAd function and contributes to the pathogenesis of UC in DKO mice.

Free Research Field

糖鎖病理学