ISSN:
1365-2036
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
: Enhanced MAdCAM-1 (mucosal addressin cell adhesion molecule-1) expression is associated with the aetiology of inflammatory bowel disease, but little is known about MAdCAM-1: regulation, or how inflammatory bowel disease therapies modulate MAdCAM-1.〈section xml:id="abs1-2"〉〈title type="main"〉Aim: To examine how agents currently used to treat inflammatory bowel disease affect MAdCAM-1: induced by tnf-α in an in vitro model of inflammatory bowel disease.〈section xml:id="abs1-3"〉〈title type="main"〉Methods: Endothelial monolayers were pretreated with dexamethasone (DEX): 5-aminosalicylic acid (5-ASA), 6-mercaptopurine (6-MP), sulfasalazine or interleukin-10: (IL-10: prior to TNF-α (20 ng/mL), and MAdCAM-1: measured by Western blotting, RT-PCR, EMSA and lymphocyte adhesion assays.〈section xml:id="abs1-4"〉〈title type="main"〉Results: MAdCAM-1: was induced dose- and time-dependently by TNF-α on endothelial cells. Either dexamethasone or IL-10: reduced TNF-α-induced MAdCAM-1: protein, mRNA and lymphocyte adhesion. However, neither 5-ASA, sulfasalazine nor 6-MP blocked MAdCAM-1 induction.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusions: Our data indicate that dexamethasone or IL-10 can exert therapeutic activity in inflammatory bowel disease through MAdCAM-1 inhibition. 5-ASA, sulfasalazine and 6-MP, while beneficial in inflammatory bowel disease, do not directly control MAdCAM-1, and are beneficial through inhibition of other inflammatory processes.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1365-2036.2001.01048.x
