PLATELET-ACTIVATING FACTOR MEDIATED DECIDUAL CYTOKINE NETWORK DURING TERM AND PRETERM PARTURITION.

Platelet-activating factor（PAF），一种潜在的脂质介质，在一系列的生产过程中被隐含，包括分离。PAF has been shown to stimulate prostaglandin E-D22-D2 production in fetal？branes and to cause myometrial contraction。PAF代谢在决定性酶中的代谢及其调制，由内毒素或细胞因子进行了调查。决定性巨噬细胞秘密的PAF-乙酰水解酶（PAF-AH）不活化的等离子体类型的活性。LPS、TNF-α和IL-1 β通过决策宏观膜抑制了PAF-AH保密。LPS抑制被IL-1 ra部分逆转，或被中性化抗TNF-α和IL-1 β抗体逆转。IL-1 β对秘密的影响被IL-1 ra驳回。IFN-γ、IL-6和IL-8也抑制了PAF-AH的保密，同时M-CSF增加了酶的保密。雌二醇被抑制了酵素的分泌物，同时也刺激了分泌物的分泌物。内皮素通过决定性宏观图来分解PAF-AH的秘密。这些观察还提供了额外的支持，即PAF在病理学上参与了由Chorioamnionitis导致的分裂或前实验室，并在fetal-maternal-decidual界面形成了一个PAF-medeated细胞因子网络。

Platelet-activating factor(PAF), a potent lipid mediator, has been implicated in a number of reproductive processes, including parturition. PAF has been shown to stimulate prostaglandin EィイD22ィエD2 production in fetal membranes and to cause myometrial contraction. PAF metabolism in the decidua and its modulation by endotoxin or cytokines has been investigated. Decidual macrophages secrete PAF-acetylhydrolase (PAF-AH) activity of the plasma type that inactivates PAF. LPS, TNF-α, and IL-1β inhibited the PAF-AH secretion by decidual macrophages. The LPS-inhibition was partially reversed by IL-1ra or by neutralizing antibodies against TNF-α and IL-1β. The effect of IL-1β on the secretion was abolished by IL-1ra. IFN-γ, IL-6, and IL-8 also inhibited the PAF-AH secretion, while M-CSF increased the enzyme secretion. Estradiol inhibited the enzyme secretion, while progesterone stimulated the secretion. Endothelins decreased the PAF-AH secretion by decidual macrophages. These observations lend additional support to the concept that PAF is pathophysiologically involved in parturition or preterm labor caused by chorioamnionitis, forming a PAF-medeated cytokine network at the fetal-maternal decidual interface.