Prostaglandin E2 production by endogenous secretion of interleukin-1 in decidual cells obtained before and after the labor

Osamu Ishihara , Hitomi Numari , Masahiro Saitoh , Yoshinori Arai , Hitoshi Takanashi , Hiroshi Kitagawa , Katsuyuki Kinoshita
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引用次数: 21

Abstract

Previous reports revealed that interleukin-1(IL-1) was involved in the process of premature labor in the cases with intrauterine infection. However, the roles of the cytokine in normal spontaneous labor remain uncertain. The present studies aimed at determining the involvement of the cytokine in prostaglandin (PG)E2 production during labor by the third trimester decidual cells. The cells were obtained at the time of normal spontaneous delivery (NVD) and elective cesarean section (ECS). The NVD cells produced significantly more amount of PGE2 than the ECS cells and the both cells responded to the addition of IL-1β to increase PGE2 production. A specific inhibitor of cyclooxygenase-2 (COX-2), NS398, decreased basal PGE2 production and inhibited the stimulatory effect of IL-1f in a dose dependent manner in NVD cells. The NVD cells secreted more amount of IL-1 fl than the ECS cells and contained more amount of preprocessed 31kD IL-1 fl inside the cells. The addition of recombinant soluble human IL-1 receptor (type I) not only blocked the effect of IL-1β on PG secretion, but significantly reduced the basal production of PGE2 by NVD cells. These results indicate that decidual PG production depends upon COX-2 after the onset of labor. Besides it seems likely that endogenously produced IL-1β may be involved in autocrine fashion in inducing COX-2 after the onset of labor.

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分娩前后蜕膜细胞内源性分泌白细胞介素-1产生前列腺素E2
以往的报道显示,白细胞介素-1(IL-1)参与了宫内感染病例的早产过程。然而,细胞因子在正常自然分娩中的作用仍不确定。目前的研究旨在确定细胞因子参与前列腺素(PG)E2生产在分娩过程中由孕晚期蜕细胞。细胞是在正常自然分娩(NVD)和选择性剖宫产(ECS)时获得的。NVD细胞比ECS细胞产生更多的PGE2,并且两种细胞对添加IL-1β有反应以增加PGE2的产生。环氧化酶-2 (COX-2)的特异性抑制剂NS398在NVD细胞中以剂量依赖的方式降低PGE2的基础生成并抑制IL-1f的刺激作用。NVD细胞比ECS细胞分泌更多的IL-1 fl,细胞内含有更多的预处理过的31kD IL-1 fl。重组可溶性人IL-1受体(I型)的加入不仅阻断了IL-1β对PG分泌的影响,而且显著降低了NVD细胞PGE2的基础生成。这些结果表明,分娩后个体PG的产生取决于COX-2。此外,内源性产生的IL-1β可能参与分娩后诱导COX-2的自分泌方式。
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