Glucocorticoids and IL‐10, but not 6‐MP, 5‐ASA or sulfasalazine block endothelial expression of MAdCAM‐1: implications for inflammatory bowel disease therapy

DOI Web Site Web Site 被引用文献4件

抄録

<jats:sec><jats:title>Background</jats:title><jats:p>: 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.</jats:p></jats:sec><jats:sec><jats:title>Aim</jats:title><jats:p>: To examine how agents currently used to treat inflammatory bowel disease affect MAdCAM‐1: induced by tnf‐α in an <jats:italic>in vitro</jats:italic> model of inflammatory bowel disease.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>: 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.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>: 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.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>: 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.</jats:p></jats:sec>

収録刊行物

被引用文献 (4)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ