肠道糖基化在确定炎症性和肿瘤性肠病患者对食物的个体反应中的作用

J. Rhodes
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引用次数: 0

摘要

目的:阐明粘膜糖基化的改变,特别是O糖基化,可能导致饮食中碳水化合物结合蛋白(凝集素)相互作用的改变。设计和方法:总结作者小组最近的文献,重点是在体外和体内证明凝集素-上皮相互作用,特别是在结肠上皮中。结果:类似的O -糖基化改变发生在炎症性疾病和癌症的结肠上皮中。它们包括O -聚糖缩短和癌胎碳水化合物抗原表达增加。花生凝集素选择性结合TF抗原,经证实可在肠内存活并显著增加上皮细胞的增殖。其他凝集素抑制增殖,例如,食用菌凝集素被内化并阻止核定位序列依赖的核蛋白进口。结论:肠上皮糖基化在…
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of intestinal glycosylation in determining individual responses to foods in inflammatory and neoplastic bowel diseases
Purpose: To illustrate the hypothesis that alterations in mucosal glycosylation, particularly O‐glycosylation, may result in altered interaction with carbohydrate‐binding proteins (lectins) in the diet.Design & methods: A summary of recent literature focussing on work by the author's group demonstrating in vitro and in vivo lectin–epithelial interactions, particularly in the colonic epithelium.Results: Similar alterations in O‐glycosylation occur in the colonic epithelium in inflammatory diseases and in cancer. They include shortening of O‐glycans and increased expression of onco‐fetal carbohydrate antigens. Peanut lectin, which selectively binds the TF antigen, is shown to survive transit through the intestine and to cause significantly increased epithelial proliferation. Other lectins inhibit proliferation, e.g. edible mushroom lectin which becomes internalised and blocks nuclear‐localising‐sequence‐dependent nuclear protein import.Conclusions: Intestinal epithelial glycosylation is commonly altered in ...
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