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Increased uterine NLRP3 inflammasome and leucocyte infiltration in a rat model of preeclampsia
American Journal of Reproductive Immunology ( IF 2.5 ) Pub Date : 2021-08-10 , DOI: 10.1111/aji.13493
Huiqian Zeng 1 , Xinjia Han 1 , Zhiqin Zhu 1 , Shengjun Yu 1 , Shanshan Mei 1 , Xi Cheng 1 , Weiqiang Zhang 1 , Guanglan Zhang 1 , Dajun Fang 1
Affiliation  

The disruption of the inflammatory microenvironment in the uterus affects pregnancy outcome. However, the exact quantification and distribution of leukocyte subpopulations in the uterus in preeclampsia (PE) have not been clearly characterized. Inflammasomes promote the release of proinflammatory cytokines interleukin (IL)-β and IL-18. A higher expression of NLRP3 inflammasome in placentas contributes to excessive inflammation in PE. However, related studies on the uterus are scarce. We aimed to investigate changes in the infiltration of leukocyte subpopulations in decidual and uterine tissues, and explore the role of activation of uterine NLRP3 inflammasomes in PE. Decidual tissues were collected from normotensive pregnant women and preeclamptic women. A PE-like model was established via administration of lipopolysaccharide to normal pregnant rats. Uterine and decidual tissues were collected from all experimental groups. It was found that the number of leukocytes was significantly elevated in decidual and uterine tissues in PE patients compared to normal controls. The leukocytes (predominantly macrophages and NK cells) particularly infiltrated into the decidua and uterine decidua in PE-like rats, and these were sparse in the myometrium. The NLRP3 immunoreactivity in the uterus was extremely little in control rats, its immunoreactivity and caspase-1 immunoreactivity were significantly elevated in the PE-like rats; the mRNA expression results also indicated an upward trend in the activation of NLRP3 inflammasomes. These results support that leucocyte infiltration in the decidua and uterine deciduas, and the activation of NLRP3 inflammasome in the uterus, which participate in the pathogenesis, are responsible for the excessive inflammation at the maternal-fetal interface during PE.

中文翻译:

在先兆子痫大鼠模型中增加子宫 NLRP3 炎性体和白细胞浸润

子宫炎症微环境的破坏会影响妊娠结局。然而,尚未明确表征先兆子痫 (PE) 中子宫内白细胞亚群的准确定量和分布。炎症小体促进促炎细胞因子白细胞介素 (IL)-β 和 IL-18 的释放。胎盘中 NLRP3 炎症小体的高表达导致 PE 过度炎症。然而,关于子宫的相关研究却很少。我们旨在研究蜕膜和子宫组织中白细胞亚群浸润的变化,并探讨子宫 NLRP3 炎性体激活在 PE 中的作用。从血压正常的孕妇和先兆子痫妇女收集蜕膜组织。通过给予正常妊娠大鼠脂多糖建立PE样模型。从所有实验组收集子宫和蜕膜组织。发现与正常对照组相比,PE患者蜕膜和子宫组织中的白细胞数量显着升高。白细胞(主要是巨噬细胞和 NK 细胞)特别浸润到 PE 样大鼠的蜕膜和子宫蜕膜中,并且这些在子宫肌层中很少见。对照大鼠子宫内NLRP3免疫反应性极低,PE样大鼠其免疫反应性和caspase-1免疫反应性显着升高;mRNA表达结果也表明NLRP3炎性体的激活呈上升趋势。这些结果支持蜕膜和子宫蜕膜中的白细胞浸润,以及参与发病机制的子宫内 NLRP3 炎性体的激活,
更新日期:2021-08-10
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