岩藻糖基化
坏死性小肠结肠炎
小肠结肠炎
粘蛋白
肠上皮
促炎细胞因子
免疫学
肠粘膜
医学
肠道通透性
内科学
胃肠病学
岩藻糖
上皮
生物
炎症
病理
生物化学
糖蛋白
作者
Xiang She,Hong‐Zhen Du,Cong Yi,Yu He,Qing Ai,Jialin Yu
标识
DOI:10.1016/j.molimm.2020.12.036
摘要
Necrotizing enterocolitis (NEC) is a devastating neonatal gastrointestinal emergency. Fucosylated glycans on intestinal epithelial cells (IECs) play a central role in the maintenance of intestinal homeostasis. Nevertheless, its association with necrotizing enterocolitis is not clear. We examined paraffin-embedded intestinal specimens from participants and found that the NEC patients showed lower intestinal epithelial fucosylation levels than the control patients. In the mouse model of NEC, the percentage of fucosylated epithelial cells (F-ECs) and ILC3s was decreased. Also, the expression levels of IL-22 and Fut2 were reduced. Moreover, the critical role of epithelial fucosylation in NEC was further confirmed by administering the anti-IL-22 antibody, which caused an increase in histological damage, body weight loss, intestinal permeability and proinflammatory cytokine release correlated with a reduction of F-ECs. Overall, intestinal fucosylation deficiency led to increased susceptibility and severity of NEC. Further studies are needed to determine whether modification of intestinal fucosylation affects the development of NEC.
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