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.

坏死性小肠结肠炎（NEC）是一种毁灭性的新生儿胃肠道急症。肠上皮细胞（IEC）上的岩藻糖基化聚糖在维持肠道稳态中发挥着核心作用。然而，其与坏死性小肠结肠炎的关系尚不清楚。我们检查了参与者的石蜡包埋肠道标本，发现 NEC 患者的肠上皮岩藻糖基化水平低于对照患者。在 NEC 小鼠模型中，岩藻糖基化上皮细胞 (F-EC) 和 ILC3 的百分比下降。此外，IL-22 和 Fut2 的表达水平也降低。此外，通过施用抗IL-22抗体进一步证实了上皮岩藻糖基化在NEC中的关键作用，该抗体导致组织学损伤、体重减轻、肠道通透性和促炎细胞因子释放的增加，与F-EC的减少相关。总体而言，肠道岩藻糖基化缺陷导致 NEC 的易感性和严重程度增加。需要进一步的研究来确定肠道岩藻糖基化的修饰是否会影响 NEC 的发展。