Titre :

Role of MAdCAM-1-Expressing High Endothelial Venule-Like Vessels in Colitis Induced in Mice Lacking Sulfotransferases Catalyzing L-Selectin Ligand Biosynthesis

Auteur(s) :

Low, Shulin [Auteur]
University of Fukui [Bunkyo]
Hirakawa, Jotaro [Auteur]
Chiba University
Hoshino, Hitomi [Auteur]
University of Fukui [Bunkyo]
Uchimura, Kenji [Auteur]
Nagoya University
Kawashima, Hiroto [Auteur]
Chiba University
Kobayashi, Motohiro [Auteur]
University of Fukui [Bunkyo]

Titre de la revue :

The Journal of Histochemistry and Cytochemistry. Official Journal of the Histochemistry Society

Nom court de la revue :

J. Histochem. Cytochem.

Numéro :

66

Pagination :

415-425

Date de publication :

2018-06

ISSN :

1551-5044

Mot(s)-clé(s) en anglais :

inflammatory bowel disease (IBD)
gut-associated lymphoid tissue (GALT)

Discipline(s) HAL :

Chimie/Chimie théorique et/ou physique

Résumé en anglais : [en]

Ulcerative colitis (UC) is a chronic inflammatory disease histologically characterized by diffuse mononuclear cell infiltrates in colonic mucosa. These inflammatory cells are considered to be recruited via high endothelial ...
Lire la suite >Ulcerative colitis (UC) is a chronic inflammatory disease histologically characterized by diffuse mononuclear cell infiltrates in colonic mucosa. These inflammatory cells are considered to be recruited via high endothelial venule (HEV)-like vessels displaying mucosal addressin cell adhesion molecule 1 (MAdCAM-1), the ligand for α4β7 integrin, and/or peripheral lymph node addressin (PNAd), an L-selectin ligand. 6- O-sulfation of N-acetylglucosamine in the carbohydrate moiety of PNAd is catalyzed exclusively by N-acetylglucosamine-6- O-sulfotransferase 1 (GlcNAc6ST-1) and GlcNAc6ST-2. To determine the role of 6- O-sulfation of N-acetylglucosamine on HEV-like vessels in UC, we used a chronic dextran sulfate sodium-induced colitis model using mice deficient in both GlcNAc6ST-1 and GlcNAc6ST-2. We found that more inflammatory cells, with expression of tumor necrosis factor α, were infiltrated in double knockout mouse colitis compared with that in wild-type mice. Moreover, the number of MAdCAM-1-positive vessels was increased in double knockout mouse colitis, and these vessels were bound by E-selectin•IgM chimeras that bind to unsulfated sialyl Lewis X (sLeX). These findings suggest that interactions between MAdCAM-1 and α4β7 integrin and/or unsulfated sLeX and L-selectin may become a dominant mechanism for inflammatory cell recruitment in the absence of 6-sulfo sLeX and contribute to more severe colitis phenotypes seen in double knockout mice.Lire moins >

Langue :

Anglais

Audience :

Non spécifiée

Établissement(s) :

CNRS
Université de Lille

Collections :

• Autres travaux scientifiques

Date de dépôt :

2020-02-12T15:11:33Z
2021-03-19T11:51:47Z