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Spontaneous embryo resorption in the mouse is triggered by embryonic apoptosis followed by rapid removal via maternal sterile purulent inflammation.
BMC Developmental Biology ( IF 1.978 ) Pub Date : 2020-01-09 , DOI: 10.1186/s12861-019-0201-0
Barbara Drews 1 , Luis Flores Landaverde 2 , Anja Kühl 3 , Ulrich Drews 4
Affiliation  

BACKGROUND In normal mammalian development a high percentage of implantations is lost by spontaneous resorption. This is a major problem in assisted reproduction and blastocyst transfer. Which embryo will be resorbed is unpredictable. Resorption is very fast, so that with conventional methods only final haemorrhagic stages are encountered. Here we describe the histology and immunohistochemistry of 23 spontaneous embryo resorptions between days 7 and 13 of murine development, which were identified by high-resolution ultrasound (US) in a previous study. RESULTS In the early resorptions detected at day 7, the embryo proper was replaced by maternal haemorrhage and a suppurate focus of maternal neutrophils. In the decidua maternal macrophages transformed to foam cells and formed a second focus of tissue dissolution. In the late resorptions detected at day 9, the embryo underwent apoptosis without involvement of maternal cells. The apoptotic embryonic cells expressed caspase 3 and embryonic blood cells developed a macrophage like phenotype. Subsequently, the wall of the embryonic vesicle ruptured and the apoptotic embryo was aborted into the uterine lumen. Abortion was initiated by degeneration of the embryonic lacunar trophoblast and dissolution of the maternal decidua capsularis via sterile inflammation and accompanied by maternal haemorrhage, invasion of the apoptotic embryo by maternal neutrophils, and contraction rings of the uterine muscle layers. CONCLUSIONS We conclude that spontaneous resorption starts with endogenous apoptosis of the embryo without maternal contribution. After break down of the foetal-maternal border, the apoptotic embryo is invaded by maternal neutrophils, aborted into the uterine lumen, and rapidly resorbed. We assume that the innate maternal unspecific inflammation is elicited by disintegrating apoptotic embryonic cells.

中文翻译:

小鼠体内的自发性胚胎吸收是由胚胎凋亡引起的,随后通过孕产妇无菌化脓性炎症迅速清除。

背景技术在正常的哺乳动物发育中,高比例的植入由于自发吸收而丢失。这是辅助生殖和胚泡转移的主要问题。哪个胚胎将被吸收是无法预测的。吸收非常快,因此使用常规方法只能遇到最后的出血阶段。在这里,我们描述了在小鼠发育的第7天到第13天之间23种自发胚胎吸收的组织学和免疫组织化学,这在先前的研究中已通过高分辨率超声(US)进行了鉴定。结果在第7天检测到的早期吸收中,正常的胚胎被母体出血和母体中性粒细胞的化脓性灶所代替。在蜕膜中,母体巨噬细胞转化为泡沫细胞并形成了组织溶解的第二个焦点。在第9天检测到的晚期吸收中,胚胎经历了凋亡,而没有母体细胞的参与。凋亡的胚胎细胞表达半胱天冬酶3,而胚胎血细胞则形成巨噬细胞样表型。随后,胚泡壁破裂,凋亡的胚胎流进子宫腔。流产是通过胚胎腔隙滋养细胞的变性和通过无菌炎症而溶解母亲蜕膜蜕膜而引发的,并伴有母亲出血,母亲中性粒细胞浸润凋亡胚胎以及子宫肌层收缩环。结论我们得出结论,自发吸收是从胚胎的内源性凋亡开始的,而没有母亲的贡献。胎儿与母亲的边界破裂后,凋亡的胚胎被母体的中性粒细胞侵袭,流进子宫腔并迅速吸收。我们假设先天的母体非特异性炎症是由凋亡的胚胎细胞解体引起的。
更新日期:2020-04-22
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