Romero R, Manogue K R, Mitchell M D, Wu Y K, Oyarzun E, Hobbins J C, Cerami A
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, CT 06510.
Am J Obstet Gynecol. 1989 Aug;161(2):336-41. doi: 10.1016/0002-9378(89)90515-2.
A growing body of evidence supports a causal link between subclinical intrauterine infection and preterm labor. The mechanisms responsible for the onset of parturition in this setting have not been elucidated. The conventional view has been that bacterial products increase prostaglandin biosynthesis by intrauterine tissues and this, in turn, leads to the onset of labor. An alternative or complementary mechanism is that microbial products activate the host monocyte-macrophage system and that cytokines released during this process signal the initiation of parturition by stimulating prostaglandin biosynthesis by intrauterine tissues. This study was conducted to determine if cachectin-tumor necrosis factor is present in the amniotic fluid of women with intraamniotic infection and whether this cytokine can alter the rate of prostaglandin biosynthesis by intrauterine tissues. Amniotic fluid from 54 women was assayed for tumor necrosis factor. Tumor necrosis factor was not detectable in the amniotic fluid of women without intraamniotic infection regardless of the presence or absence of term or preterm labor. On the other hand, the amniotic fluid of 11 of 15 women with preterm labor and intraamniotic infection had measurable tumor necrosis factor. This cytokine stimulated prostaglandin E2 biosynthesis by amnion cells in monolayer culture in a dose-dependent fashion. These data support the concept that macrophage activation is involved in the onset of human parturition in the setting of infection. We propose that the host (fetus and/or mother) signals the onset of parturition through the secretion of inflammatory cytokines released in response to bacterial invasion.
越来越多的证据支持亚临床宫内感染与早产之间存在因果关系。这种情况下导致分娩开始的机制尚未阐明。传统观点认为，细菌产物会增加宫内组织中前列腺素的生物合成，进而导致分娩开始。另一种或补充性机制是，微生物产物激活宿主单核细胞 - 巨噬细胞系统，在此过程中释放的细胞因子通过刺激宫内组织中前列腺素的生物合成来发出分娩开始的信号。本研究旨在确定恶病质素 - 肿瘤坏死因子是否存在于羊膜腔内感染女性的羊水当中，以及这种细胞因子是否会改变宫内组织中前列腺素的生物合成速率。对54名女性的羊水进行了肿瘤坏死因子检测。无论足月或早产情况如何，未发生羊膜腔内感染的女性羊水中均未检测到肿瘤坏死因子。另一方面，15名早产且伴有羊膜腔内感染的女性中，有11名女性的羊水检测到了可测量的肿瘤坏死因子。这种细胞因子以剂量依赖的方式刺激单层培养的羊膜细胞合成前列腺素E2。这些数据支持巨噬细胞激活参与感染情况下人类分娩开始的概念。我们提出，宿主（胎儿和/或母亲）通过分泌因细菌入侵而释放的炎性细胞因子来发出分娩开始的信号。
