宫内感染/炎症 (IUI) 是一种常见的妊娠并发症，可导致早产和胎儿炎症。如何在母胎界面调节炎症尚未解决。我们将脂多糖诱导的早产恒河猴 IUI 模型中的羊膜（与羊水接触的胎儿组织）的转录组学与人类绒毛膜羊膜炎队列进行了比较。批量 RNA 测序 (RNA-seq) 羊膜转录组图谱在恒河猴和人类受试者中非常相似，表明 IL1 和 IL6 等关键临产介导基因的诱导依赖于核因子 κB (NF-κB) 信号传导，并可通过抗肿瘤坏死因子（TNF）抗体阿达木单抗。阿达木单抗可部分恢复 IUI 对胶原生物合成的抑制作用。有趣的是，单细胞转录组学、流式细胞术和免疫组织学表明，在人类和恒河猴的 IUI 过程中，羊膜间充质细胞 (AMC) 的一部分会增加 CD14 和其他骨髓细胞标记物。我们的数据表明 CD14 AMC 代表母胎界面处激活的 AMC。© 2023 作者。

Intrauterine infection/inflammation (IUI) is a frequent complication of pregnancy leading to preterm labor and fetal inflammation. How inflammation is modulated at the maternal-fetal interface is unresolved. We compared transcriptomics of amnion (a fetal tissue in contact with amniotic fluid) in a preterm Rhesus macaque model of IUI induced by lipopolysaccharide with human cohorts of chorioamnionitis. Bulk RNA sequencing (RNA-seq) amnion transcriptomic profiles were remarkably similar in both Rhesus and human subjects and revealed that induction of key labor-mediating genes such as IL1 and IL6 was dependent on nuclear factor κB (NF-κB) signaling and reversed by the anti-tumor necrosis factor (TNF) antibody Adalimumab. Inhibition of collagen biosynthesis by IUI was partially restored by Adalimumab. Interestingly, single-cell transcriptomics, flow cytometry, and immunohistology demonstrated that a subset of amnion mesenchymal cells (AMCs) increase CD14 and other myeloid cell markers during IUI both in the human and Rhesus macaque. Our data suggest that CD14+ AMCs represent activated AMCs at the maternal-fetal interface.© 2023 The Author(s).