Function of the glycosyltransferase GnT-V in colitis
Function of the glycosyltransferase GnT-V in colitis
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糖基转移酶 GnT-V 在结肠炎中的功能
DOI：
10.1007/s00535-015-1156-y
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Motohiro Nonaka
中科院分区：
文献类型：
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作者：
Motohiro Nonaka
炎症性肠病(IBD)，如克罗恩病和溃疡性结肠炎，以胃肠道慢性炎症为特征。虽然IBD的确切发病机制尚未完全阐明，但人们普遍认为宿主遗传和肠道微生物区系共同触发了这两种疾病。在各种自发的、诱导的和遗传的IBD动物模型中，使用葡聚糖硫酸钠(DSS)可能是最常见的诱导小鼠结肠炎的方法[5]。DSS驱动的结肠炎可能发生的一系列事件包括结肠内粘液屏障受损、细菌渗透和宿主免疫细胞对细菌的识别。鉴于DSS诱导的结肠炎即使在T和B细胞缺陷的小鼠中也可以复制[6]，先天免疫细胞(如巨噬细胞)的激活以及一组特定细胞因子的分泌可能是疾病诱导的关键事件。在本期《胃肠病学杂志》中，Shinzaki等人[7]证明了基因转移和随后的N-乙酰氨基葡萄糖转移酶V(GnT-V)的过度表达损害了小鼠的巨噬细胞功能，GnT-V是一种催化N-糖链上b1，6N-乙酰氨基葡萄糖(GlcNAc)分支的酶。当用DSS处理GnT-V转基因(TG)小鼠时，分离的巨噬细胞
Inflammatory bowel diseases (IBDs), such as Crohn’s disease and ulcerative colitis, are characterized by chronic inflammation in the gastrointestinal tract. Although the precise pathogenesis of IBD is not fully clarified, it is widely accepted that host genetics and intestinal microbiota collectively trigger both diseases. Among the variety of spontaneous, inducible, and genetic animal models of IBD [1–4], usage of dextran sodium sulfate (DSS) is perhaps the most common method to induce colitis in mice [5]. A possible sequence of events in DSS-driven colitis involves damage to the colonic inner mucus barrier, bacterial infiltration, and bacterial recognition by host immune cells. Given that DSS-induced colitis is reproducible even in T-and B-cell-deficient mice [6], activation of innate immune cells (eg macrophages) followed by secretion of a particular set of cytokines are likely critical events in disease induction.In this issue of Journal of Gastroenterology, Shinzaki et al.[7] demonstrated that gene transfer and subsequent overexpression of N-acetylglucosaminyltransferase V (GnT-V), an enzyme that catalyzes b1, 6N-acetylglucosamine (GlcNAc) branching on N-glycans, impaired macrophage function in mice. When GnT-V transgenic (Tg) mice were treated with DSS, isolated macrophages