Analysis of the innate immune receptor NOD1 and its ligands as a novel cause for the development of the intrauterine fetal growth restriction

先天免疫受体 NOD1 及其配体作为宫内胎儿生长受限发生的新原因的分析

• 批准号: 24659509
• 负责人: HARA TOSHIRO
• 金额: $ 2.33万
• 依托单位: Kyushu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24659509/
• 关键词: 自然免疫; 子宮内胎児発育遅延; 子宮内胎児死亡; Nod1; 周産期; 子宮内発育遅延; 自然免疫受容体; NOD1

Nod1 (nucleotide-binding oligomerization domain containing 1) is one of the pattern recognition receptors that play an important role in the induction of innate immune and inflammatory responses. However, little is known regarding the effects of direct activation of Nod1 on fetus or newborn. In this study, we demonstrated that administration of Nod1 ligand to pregnant mice induced intrauterine fetal death and growth restriction. We also found that fetuses were affected by transplacental passage of maternal Nod1 ligand. We examined the role of Nod1 signaling in a fetal mouse with a focus on the development of vasculopathy. Our observation suggests a possible link between Nod1 ligands-mediated activation of the innate immune system in fetus and IUGR and might offer a new strategy to improve the long-term cardiovascular health of IUGR cases.

Nod1 （nucleotide-binding oligomerization domain containing 1）是一种模式识别受体，在诱导先天免疫和炎症反应中发挥重要作用。然而，直接激活Nod1对胎儿或新生儿的影响尚不清楚。在这项研究中，我们证明给妊娠小鼠注射Nod1配体会导致宫内胎儿死亡和生长受限。我们还发现胎儿受母体Nod1配体经胎盘传递的影响。我们研究了Nod1信号在胎儿小鼠血管病变发展中的作用。我们的观察表明Nod1配体介导的胎儿先天免疫系统激活与IUGR之间可能存在联系，并可能为改善IUGR病例的长期心血管健康提供新的策略。

项目成果

Innate immunity and infection in the newborn

新生儿的先天免疫和感染

• 发表时间: 2013
• 作者: Kitajima J;Inoue H;Ohga S;Kinjo T;Ochiai M;Yoshida T;Kusuhara K;Hara T;Hara T.
• 通讯作者: Hara T.

Survival and neurodevelopmental outcome of preterm infants born at 22-24 weeks of gestational age.

胎龄 22-24 周出生的早产儿的生存和神经发育结果。

• DOI: 10.1159/000355818
• 发表时间: 2014
• 期刊: Neonatology
• 影响因子: 2.5
• 作者: Ochiai M;Kinjo T;Takahata Y;Iwayama M;Abe T;Ihara K;Ohga S;Fukushima K;Kato K;Taguchi T;Hara T
• 通讯作者: Hara T

Activation of an Innate Immune Receptor, Nod1, Accelerates Atherogenesis in Apoe-/- Mice

• DOI: 10.4049/jimmunol.1302841
• 发表时间: 2015-01-15
• 期刊: JOURNAL OF IMMUNOLOGY
• 影响因子: 4.4
• 作者: Kanno, Shunsuke;Nishio, Hisanori;Hara, Toshiro
• 通讯作者: Hara, Toshiro

Differential transmission and postnatal outcome in triplets with congenital cytomegalovirus infection

先天性巨细胞病毒感染三胞胎的差异传播和产后结局

• DOI: 10.2350/11-05-1034-cr.1
• 发表时间: 2011
• 期刊: Pediatr Development Pathol
• 作者: Kitajima J;Inoue H;Ohga S;Kinjo T;Ochiai M;Yoshida T;Kusuhara K;Hara T
• 通讯作者: Hara T

Activation of Nod1-mediated innate immunity accelerates autherogenesis

Nod1 介导的先天免疫的激活加速自体动脉粥样硬化形成

• 发表时间: 2013
• 作者: Kanno S;Nishio H;Sueishi K;Hara T.
• 通讯作者: Hara T.