Nakabayashi M, Sakura M, Takeda Y, Sato K
Tokyo Women's Medical College, Department of Obstetrics and Gynecology, Japan.
Am J Reprod Immunol. 1998 May;39(5):329-34. doi: 10.1111/j.1600-0897.1998.tb00526.x.
The primary defect of placental development in preeclampsia is speculated to occur at midtrimester gestation. Abnormal feto-maternal immune reactions have been considered as factors in such defective placentation.
Midtrimester amniotic fluid specimens were retrospectively identified as coming from gestations that later had severe preeclampsia develop, gestations with normal outcomes, and gestations measured for cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin (IL-1 beta, IL-6, and IL-8). The effect of each cytokine on thrombomodulin levels was tested in cultured trophoblast cells.
Among the measured cytokines, IL-6 and IL-8 were significantly elevated in the midtrimester amniotic fluid of the future preeclamptic group. Trophoblasts stimulated with TNF-alpha plus IL-6 had significantly decreased levels of cellular thrombomodulin compared to those without cytokine addition.
Elevated cytokines in midtrimester amniotic fluid suggest an abnormal fetomaternal immune response occurring before the clinical manifestation of preeclampsia. Cytokine-induced suppression of thrombomodulin in trophoblasts may be directly involved in the pathogenesis of preeclampsia.
子痫前期胎盘发育的主要缺陷推测发生在妊娠中期。异常的母胎免疫反应被认为是导致这种胎盘形成缺陷的因素。
回顾性地确定妊娠中期羊水样本分别来自后来发生重度子痫前期的妊娠、结局正常的妊娠以及检测细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素（IL-1β、IL-6和IL-8）的妊娠。在培养的滋养层细胞中测试每种细胞因子对血栓调节蛋白水平的影响。
在所检测的细胞因子中，未来子痫前期组妊娠中期羊水中IL-6和IL-8显著升高。与未添加细胞因子的滋养层细胞相比，用TNF-α加IL-6刺激的滋养层细胞中细胞血栓调节蛋白水平显著降低。
妊娠中期羊水中细胞因子升高表明在子痫前期临床表现之前发生了异常的母胎免疫反应。细胞因子诱导的滋养层细胞中血栓调节蛋白的抑制可能直接参与子痫前期的发病机制。
