ACE2 Is Expressed in Immune Cells That Infiltrate the Placenta in Infection-Associated Preterm Birth.
ACE2 Is Expressed in Immune Cells That Infiltrate the Placenta in Infection-Associated Preterm Birth.
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ACE2在与感染相关的早产中浸润胎盘的免疫细胞中表达。
作者：
Lye P;Dunk CE;Zhang J;Wei Y;Nakpu J;Hamada H;Imperio GE;Bloise E;Matthews SG;Lye SJ
COVID-19与早产（PTB）发生率增加有关。我们评估了SARS-CoV-2进入胎盘的途径。收集来自PTB伴或不伴绒毛膜炎（ChA）或足月妊娠（n = 12/13/组）的胎盘。从健康孕妇（n = 6）收集外周血。用脂多糖（LPS，模拟细菌感染）处理妊娠中期胎盘外植体（16-20周，n = 5/组），并评估ACE 2、CCL 2、IL-6/8和TNFα mRNA。ChA-胎盘显示ACE 2和CCL 2 mRNA表达增加（p < 0.05）。LPS可增加胎盘组织中细胞因子和ACE 2 mRNA的表达。胎盘ACE 2蛋白定位于合体滋养层、胎儿内皮、绒毛外滋养层和绒毛间质内的免疫细胞亚群（M1/M2巨噬细胞和中性粒细胞）。ChA-胎盘中M1巨噬细胞和中性粒细胞的数量显著增加（p < 0.001）。来自孕妇的外周免疫细胞亚群表达ACE 2 mRNA和蛋白。与淋巴细胞或单核细胞相比，粒细胞中ACE 2蛋白表达呈阳性的比例更大。这些数据表明，在妊娠合并ChA时，母体循环中的ACE 2阳性免疫细胞有可能将SARS-CoV-2病毒运输到胎盘，并增加垂直传播到胎盘/胎儿的风险。
COVID-19 is associated with increased incidence of preterm birth (PTB). We assessed pathways by which SARS-CoV-2 could access the placenta. Placentae, from PTB with or without chorioamnionitis (ChA), or from term pregnancies (n = 12/13/group) were collected. Peripheral blood was collected from healthy pregnant women (n = 6). Second trimester placental explants (16–20 weeks, n = 5/group) were treated with lipopolysaccharide (LPS, to mimic bacterial infection) and ACE2, CCL2, IL-6/8 and TNFα mRNA was assessed. ChA-placentae exhibited increased ACE2 and CCL2 mRNA expression (p < 0.05). LPS increased cytokine and ACE2 mRNA in placental explants. Placental ACE2 protein localized to syncytiotrophoblast, fetal endothelium, extravillous trophoblast and in immune cells-subsets (M1/M2 macrophage and neutrophils) within the villous stroma. Significantly increased numbers of M1 macrophage and neutrophils were present in the ChA-placenta (p < 0.001). Subsets of peripheral immune cells from pregnant women express the ACE2 mRNA and protein. A greater fraction of granulocytes was positive for ACE2 protein expression compared to lymphocytes or monocytes. These data suggest that in pregnancies complicated by ChA, ACE2 positive immune cells in the maternal circulation have the potential to traffic SARS-CoV-2 virus to the placenta and increase the risk of vertical transmission to the placenta/fetus.
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