SARS-CoV-2 Infection during Delivery Causes Histopathological Changes in the Placenta

Diseases Pub Date : 2024-07-02 DOI:10.3390/diseases12070142
Jędrzej Borowczak, Agnieszka Gąsiorek-Kwiatkowska, Krzysztof Szczerbowski, Mateusz Maniewski, Marek Zdrenka, Marta Szadurska-Noga, Karol Gostomczyk, Paula Rutkiewicz, Katarzyna Olejnik, Wojciech Cnota, Magdalena Karpów-Greiner, Wojciech Knypiński, Marta I Sekielska-Domanowska, Grzegorz Ludwikowski, Mariusz Dubiel, Łukasz Szylberg, Magdalena Bodnar
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Abstract

Background: SARS-CoV-2 can damage human placentas, leading to pregnancy complications, such as preeclampsia and premature birth. This study investigates the histopathological changes found in COVID-19-affected placentas. Materials and Methods: This study included 23 placentas from patients with active COVID-19 during delivery and 22 samples from patients without COVID-19 infection in their medical history. The samples underwent histopathological examination for pathology, such as trophoblast necrosis, signs of vessel damage, or fetal vascular malperfusion. Results: Newborns from the research group have lower weights and Apgar scores than healthy newborns. In the COVID-19 group, calcifications and collapsed intervillous space were more frequent, and inflammation was more severe than in the healthy group. At the same time, the placenta of SARS-CoV-2-positive patients showed signs of accelerated vascular maturation. Trophoblast necrosis was found only in the placentas of the research group. The expression of CD68+ was elevated in the COVID-19 cohort, suggesting that macrophages constituted a significant part of the inflammatory infiltrate. The increase in lymphocyte B markers was associated with placental infarctions, while high levels of CD3+, specific for cytotoxic T lymphocytes, correlated with vascular injury. Conclusions: SARS-CoV-2 is associated with pathological changes in the placenta, including trophoblast necrosis, calcification, and accelerated villous maturation. Those changes appear to be driven by T cells and macrophages, whose increased expression reflects ongoing histiocytic intervillositis in the placenta.
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分娩时感染 SARS-CoV-2 导致胎盘组织病理学变化
背景:SARS-CoV-2 可损害人类胎盘,导致妊娠并发症,如子痫前期和早产。本研究调查了受 COVID-19 影响的胎盘的组织病理学变化。材料和方法:本研究包括 23 份来自分娩过程中 COVID-19 活动患者的胎盘样本和 22 份来自无 COVID-19 感染病史患者的胎盘样本。对样本进行组织病理学检查,以确定是否存在滋养层坏死、血管损伤或胎儿血管灌注不良等病理现象。结果研究组新生儿的体重和阿普加评分均低于健康新生儿。与健康组相比,COVID-19 研究组的钙化和绒毛间隙塌陷更为常见,炎症也更为严重。同时,SARS-CoV-2 阳性患者的胎盘显示出血管加速成熟的迹象。仅在研究组的胎盘中发现滋养细胞坏死。在 COVID-19 研究组中,CD68+ 的表达升高,表明巨噬细胞在炎症浸润中占了很大一部分。淋巴细胞 B 标记的增加与胎盘梗塞有关,而细胞毒性 T 淋巴细胞特异性 CD3+ 的高水平与血管损伤有关。结论SARS-CoV-2 与胎盘的病理变化有关,包括滋养层坏死、钙化和绒毛成熟加速。这些变化似乎是由 T 细胞和巨噬细胞驱动的,其表达的增加反映了胎盘中正在发生的组织细胞间质炎。
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