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首页> 美国卫生研究院文献>The Journal of Immunology Author Choice >Activation of Nod1 Signaling Induces Fetal Growth Restriction and Death through Fetal and Maternal Vasculopathy
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Activation of Nod1 Signaling Induces Fetal Growth Restriction and Death through Fetal and Maternal Vasculopathy

机译：Nod1信号的激活通过胎儿和母体血管病变诱导胎儿生长受限和死亡

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Intrauterine fetal growth restriction (IUGR) and death (IUFD) are both serious problems in the perinatal medicine. Fetal vasculopathy is currently considered to account for a pathogenic mechanism of IUGR and IUFD. We previously demonstrated that an innate immune receptor, the nucleotide-binding oligomerization domain-1 (Nod1), contributed to the development of vascular inflammations in mice at postnatal stages. However, little is known about the deleterious effects of activated Nod1 signaling on embryonic growth and development. We report that administration of FK565, one of the Nod1 ligands, to pregnant C57BL/6 mice induced IUGR and IUFD. Mass spectrometry analysis revealed that maternally injected FK565 was distributed to the fetal tissues across placenta. In addition, maternal injection of FK565 induced robust increases in the amounts of CCL2, IL-6, and TNF proteins as well as NO in maternal, placental and fetal tissues. Nod1 was highly expressed in fetal vascular tissues, where significantly higher levels of CCL2 and IL-6 mRNAs were induced with maternal injection of FK565 than those in other tissues. Using Nod1-knockout mice, we verified that both maternal and fetal tissues were involved in the development of IUGR and IUFD. Furthermore, FK565 induced upregulation of genes associated with immune response, inflammation, and apoptosis in fetal vascular tissues. Our data thus provided new evidence for the pathogenic role of Nod1 in the development of IUGR and IUFD at the maternal-fetal interface.
机译：宫内胎儿生长受限（IUGR）和死亡（IUFD）都是围产期医学中的严重问题。胎儿血管病变目前被认为是IUGR和IUFD的致病机制。我们以前证明，先天性免疫受体，核苷酸结合寡聚域1（Nod1），在出生后的小鼠中促进了血管炎症的发展。但是，关于激活的Nod1信号传导对胚胎生长和发育的有害影响知之甚少。我们报告到怀孕的C57BL / 6小鼠FK565，Nod1配体之一的管理诱导了IUGR和IUFD。质谱分析表明，母体注射的FK565分布在整个胎盘的胎儿组织中。此外，母体注射FK565会导致母体，胎盘和胎儿组织中CCL2，IL-6和TNF蛋白以及NO的含量大量增加。 Nod1在胎儿血管组织中高表达，其中母体注射FK565诱导的CCL2和IL-6 mRNA水平明显高于其他组织。使用Nod1基因敲除小鼠，我们验证了母体和胎儿组织都参与了IUGR和IUFD的发展。此外，FK565诱导与胎儿血管组织免疫应答，炎症和细胞凋亡相关的基因上调。因此，我们的数据为Nod1在母胎界面IUGR和IUFD发育中的致病作用提供了新的证据。

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