Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Pediatrics, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; National Clinical Research Center for Child Health and Disorder, Chongqing, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing, China.
Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China; Department of Pediatrics, Shenzhen University General Hospital, Shenzhen, Guangdong, China; Chongqing Key Laboratory of Pediatrics, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; National Clinical Research Center for Child Health and Disorder, Chongqing, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing, China.
Mol Immunol. 2021 Mar;131:23-32. doi: 10.1016/j.molimm.2020.12.036. Epub 2021 Jan 16.
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）是一种严重的新生儿胃肠道急症。肠道上皮细胞（IECs）上的岩藻糖基化聚糖在维持肠道内稳态中发挥核心作用。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标本，发现 NEC 患者的肠道上皮岩藻糖基化水平低于对照组患者。在 NEC 的小鼠模型中，岩藻糖化上皮细胞（F-ECs）和 ILC3 的比例减少，IL-22 和 Fut2 的表达水平降低。此外，通过给予抗 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，这导致组织学损伤增加、体重减轻、肠道通透性增加和促炎细胞因子释放，与 F-ECs 的减少相关。总的来说，肠道岩藻糖基化不足导致 NEC 的易感性和严重程度增加。需要进一步研究以确定肠道岩藻糖基化的改变是否会影响 NEC 的发展。
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