Translational Medicine, The Hospital for Sick Children, Toronto, ON M5G0A4, Canada.
Division of General and Thoracic Surgery, The Hospital for Sick Children, Toronto, ON M5G1X8, Canada.
Dis Model Mech. 2019 Dec 9;12(12):dmm040998. doi: 10.1242/dmm.040998.
Major risk factors for necrotizing enterocolitis (NEC) are formula feeding and prematurity; however, their pathogenic mechanisms are unknown. Here, we found that insufficient arginine/nitric oxide synthesis limits blood flow in the intestinal microvasculature, leading to hypoxia, mucosal damage and NEC in the premature intestine after formula feeding. Formula feeding led to increased intestinal hypoxia in pups at postnatal day (P)1 and P5, but not in more mature pups at P9. Accordingly, blood flow in the intestinal microvasculature increased after formula feeding in P9 pups only. mRNA profiling revealed that regulators of arginine/nitric oxide synthesis are at higher levels in endothelial cells of the intestine in P9 than in P1 pups. Importantly, arginine supplementation increased intestinal microvasculature blood flow and prevented NEC, whereas an arginine antagonist exacerbated NEC. Our results suggest that balancing intestinal oxygen demand and supply in the premature intestine by modulating arginine/nitric oxide could be used to prevent NEC.This article has an associated First Person interview with the first author of the paper.
主要的坏死性小肠结肠炎(NEC)风险因素是配方奶喂养和早产;然而,其发病机制尚不清楚。在这里,我们发现,精氨酸/一氧化氮合成不足限制了肠道微血管的血流,导致在配方奶喂养后的早产儿肠道中缺氧、黏膜损伤和 NEC。配方奶喂养导致出生后第 1 天(P)1 和 P5 的幼崽肠道缺氧增加,但在更成熟的 P9 幼崽中没有增加。因此,仅在 P9 幼崽中,配方奶喂养后肠道微血管的血流增加。mRNA 谱分析显示,P9 幼崽肠道内皮细胞中精氨酸/一氧化氮合成的调节剂水平高于 P1 幼崽。重要的是,精氨酸补充增加了肠道微血管的血流,预防了 NEC,而精氨酸拮抗剂则加重了 NEC。我们的研究结果表明,通过调节精氨酸/一氧化氮来平衡早产儿肠道的氧气需求和供应,可能用于预防 NEC。本文有一篇与论文第一作者的相关第一人称访谈。