Placental Macrophages Following Maternal SARS-CoV-2 Infection in Relation to Placental Pathology
Placental Macrophages Following Maternal SARS-CoV-2 Infection in Relation to Placental Pathology
复制标题
DOI：
10.3389/fviro.2022.813312
复制
发表时间：
2022-02-08
期刊：
影响因子：
--
通讯作者：
Heazell, Alexander E. P.
中科院分区：
文献类型：
--
作者：
Sharps, Megan C.;Garrod, Ainslie;Heazell, Alexander E. P.
导读：2019年12月，一种新型冠状病毒SARS-CoV-2被鉴定出来。虽然孕妇似乎有严重感染、早产和死产的风险，但尚不清楚胎盘功能障碍是否是妊娠期间母体SARS-CoV-2感染的一致特征。我们的目的是描述在怀孕期间感染COVID-19的妇女的胎盘中的免疫反应，并调查是否有任何相关的形态学变化。方法：将怀孕期间COVID-19检测阳性的妇女的胎盘与同期对照组进行比较，这些对照组在怀孕期间没有感染COVID-19。每个胎盘的样本被送去进行组织病理学分析或进行CD 163、CD 20、CD 3、CD 31和SARS-CoV-2刺突蛋白的免疫组织化学染色。结果COVID后组中CD 163+巨噬细胞的数量显著增加（p = 0.0020）。与对照组相比，COVID后组的CD 3+、CD 20+细胞百分比无差异，但胎盘血管分布增加（p = 0.026）。发送进行EM分析的样品之间未观察到结构差异。然而，观察到COVID后组的其中一个胎盘在合体滋养层中有几个大的亚顶端空泡。我们在空泡内没有观察到任何病毒粒子，并且SARS-CoV-2刺突蛋白染色对样品呈阴性。组织学研究表明，在这组样本中，没有由母体COVID-19感染引起的特异性胎盘病理学。结果：在COVID后组中，CD 163+巨噬细胞的数量显著增加（p = 0.0020）。与对照组相比，COVID后组的CD 3+、CD 20+细胞百分比无差异，但胎盘血管分布增加（p = 0.026）。发送进行EM分析的样品之间未观察到结构差异。然而，观察到COVID后组的其中一个胎盘在合体滋养层中有几个大的亚顶端空泡。我们在空泡内没有观察到任何病毒粒子，并且SARS-CoV-2刺突蛋白染色对样品呈阴性。组织学研究表明，在这组样本中没有由母体COVID-19感染引起的特异性胎盘病理。结论：这项研究没有证实先前的研究，这些研究描述了患有COVID-19的妇女中母体和胎儿血管灌注不良和胎盘炎的病例可能增加，这些病例与不良妊娠结局相关。目前尚不清楚观察到的异常是否由母体感染引起，或者母体感染是否加剧了现有的胎盘病理;了解为什么一些胎盘产生这些异常是一个关键目标。
Introduction: In December 2019, a novel coronavirus, SARS-CoV-2, was identified. Whilst pregnant women appear to be at risk of severe infection, pre-term birth, and stillbirth, it is unclear whether placental dysfunction is a consistent feature of maternal SARS-CoV-2 infection during pregnancy. We aim to describe the immune response in placentas of women who had COVID-19 infection during pregnancy and investigate whether there are any associated morphological changes.Methods: The placentas of women testing positive for COVID-19 during their pregnancy were compared to contemporaneous controls who were not known to have had COVID-19 during pregnancy. Samples of each placenta were sent for histopathological analysis or underwent immunohistochemical staining for CD163, CD20, CD3, CD31, and SARS-CoV-2 spike protein. A subset of samples were sent for transmission electron microscopy.Results There was a significant increase in the number of CD163+ macrophages in the Post COVID group (p = 0.0020). There was no difference in the percentage of CD3+, CD20+ cells, but there was an increase in placental vascularity in the Post COVID group compared to controls (p = 0.026). There were no structural differences observed between the samples sent for EM analysis. However, one of the placentas from the Post COVID group was seen to have several large sub-apical vacuoles in the syncytiotrophoblast. We did not observe any virions within the vacuoles and SARS-CoV-2 spike protein staining was negative for the sample. Histopathological investigations indicated that there was no specific placental pathology caused by maternal COVID-19 infection in this cohort of samples.Results: There was a significant increase in the number of CD163+ macrophages in the Post COVID group (p = 0.0020). There was no difference in the percentage of CD3+, CD20+ cells, but there was an increase in placental vascularity in the Post COVID group compared to controls (p = 0.026). There were no structural differences observed between the samples sent for EM analysis. However, one of the placentas from the Post COVID group was seen to have several large sub-apical vacuoles in the syncytiotrophoblast. We did not observe any virions within the vacuoles and SARS-CoV-2 spike protein staining was negative for the sample. Histopathological investigations indicated that there was no specific placental pathology caused by maternal COVID-19 infection in this cohort of samples.Conclusions: This study did not confirm previous studies which describe a possible increase in cases of both maternal and fetal vascular malperfusion, and placentitis in women who had COVID-19, which were seen in association with adverse pregnancy outcomes. It remains unclear whether observed abnormalities are caused by maternal infection, or whether maternal infection exacerbates existing placental pathology; understanding why some placentas generate these abnormalities is a key goal.