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

Platelet-activating factor(PAF), a potent lipid mediator，已implicated in a number of reproductive processes包含parturition. PAF been shown to stimulate prostaglandin E - D22 - D2 production in fetalmembranes and to cause myometrial contraction. PAF metabolism in the decidua and its modulation byendotoxin or cytokines has been investigated. Decidual macrophages secrete PAF-acetylhydrolase（af - 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伊尔-1ra or neutralizing antibodies against TNF-α and IL-1β。The effect of IL-1β on The伊尔-1ra， IFN-γ，伊尔-6，伊尔-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 paaf - ah secretion by decidualmacrophages.这些observations lend additional support to the concept that PAF ispathophysiologically involved in parturition or preterm labor caused by chorioamnionitis，forming a PAF-medeated cytokine network at the fetal-maternal decidual interface。

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.