Given the high prevalence of HIV infection and pre-eclampsia (PE) in South Africa, this study evaluated and compared the placental immunostaining of progesterone (P) and progesterone receptors (PR) in the synergy of HIV-infected PE compared to normotensive pregnant women using immunohistochemistry interfaced with morphometric image analysis. Progesterone immunostaining was expressed widely across exchange and conducting villi within mesenchymal, endothelial, and trophoblast cells. In contrast, PR was expressed within syncytiotrophoblasts and was absent within endothelial cells. In exchange villi, P and PR immuno-expression was significantly lower in PE compared to the normotensive group (p = < 0.0001 and p = < 0.0001, respectively) and within the early-onset pre-eclampsia (EOPE) compared to the late-onset pre-eclampsia (LOPE) group (p = < 0.0001 and p = < 0.0001, respectively). Progesterone immuno-expression was significantly lower in the HIV+ compared to the HIV− group (p = < 0.0001), whilst PR was non-significant. In conducting villi, P and PR immuno-expression was significantly lower in the EOPE compared to the LOPE group (p = < 0.0001 and p = < 0.0001, respectively) and in the HIV+ compared to the HIV− group (p = < 0.0001 and p = 0.0009, respectively). Progesterone immuno-expression was slightly higher in the PE compared to normotensive group, and PR immuno-expression was non-significant. There was a significant difference between P and PR within exchange versus conducting villi regardless of pregnancy type, with villi type accounting for 34.47% and 15.28% of total variance for P and PR, respectively. Placental P and PR immuno-expression is downregulated in the duality of PE and HIV+ infection. The use of combined antiretroviral therapy (cART) may result in defective P synthesis, which causes insufficient binding to its receptors. Consequently, PI3K/AKT, JAK-STAT, and MAPK signalling pathways are affected, impairing trophoblast invasion and leading to pre-eclampsia development. Notably, the decrease in P and PR immuno-expression in EOPE validates their effect on placentation.

鉴于南非 HIV 感染和先兆子痫 (PE) 的高患病率，本研究评估并比较了 HIV 感染 PE 与血压正常孕妇的胎盘孕酮 (P) 和孕酮受体 (PR) 协同作用的免疫染色使用免疫组织化学与形态测量图像分析相结合。黄体酮免疫染色在间充质细胞、内皮细胞和滋养层细胞内的交换和传导绒毛中广泛表达。相反，PR 在合体滋养细胞内表达，在内皮细胞内不表达。在交换绒毛中，与血压正常组相比，PE 中的 P 和 PR 免疫表达显着较低（分别为p  = < 0.0001 和p  = < 0.0001），并且与晚发性先兆子痫 (EOPE) 相比，早发性先兆子痫 (EOPE) 中的 P 和PR 免疫表达显着较低。发病先兆子痫 (LOPE) 组（分别为p  = < 0.0001 和p  = < 0.0001）。与 HIV− 组相比，HIV+ 组中的孕酮免疫表达显着降低 ( p  = < 0.0001)，而 PR 不显着。在进行绒毛时，与 LOPE 组相比，EOPE 组中的 P 和 PR 免疫表达显着较低（分别为p  = < 0.0001 和p  = < 0.0001），并且与 HIV− 组相比，HIV+ 组中的 P 和 PR 免疫表达显着较低（p  = < 0.0001 和p = < 0.0001）。 p  = 0.0009，分别）。与血压正常组相比，PE组中孕酮免疫表达略高，而PR免疫表达不显着。无论妊娠类型如何，交换内的 P 和 PR 与进行绒毛移植之间存在显着差异，绒毛类型分别占 P 和 PR 总方差的 34.47% 和 15.28%。在 PE 和 HIV+ 感染的双重性中，胎盘 P 和 PR 免疫表达下调。使用联合抗逆转录病毒疗法 (cART) 可能会导致 P 合成缺陷，从而导致与其受体的结合不足。因此，PI3K/AKT、JAK-STAT 和 MAPK 信号通路受到影响，损害滋养层侵袭并导致先兆子痫的发生。值得注意的是，EOPE 中 P 和 PR 免疫表达的减少证实了它们对胎盘的影响。