Peltier Morgan R
Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, UT 84132, USA.
Reprod Biol Endocrinol. 2003 Dec 2;1:122. doi: 10.1186/1477-7827-1-122.
During pregnancy there is an alteration in maternal immunity within the uterus where innate, proinflammatory immune responses are tightly regulated to prevent immunological rejection of the fetal allograft. Disruption of the delicate balance of cytokines by bacteria or other factors increases the production of proinflammatory cytokines at the maternal-fetal interface and activates the parturition mechanism prematurely. Despite years of searching, there is still no broadly effective strategy for preventing preterm labor and most therapies are directed at inhibiting myometrial contractions and improving neonatal outcome. Recent studies with progestins and interleukin-10 (IL-10), however, are showing promise in randomized clinical trials and animal studies. Furthermore, the identification of the Toll-like receptors as upstream mediators of inflammation may offer alternative therapeutic targets for preventing this common pregnancy complication.
在怀孕期间,子宫内的母体免疫会发生改变,其中先天性促炎免疫反应受到严格调控,以防止对胎儿异体移植物的免疫排斥。细菌或其他因素破坏细胞因子的微妙平衡,会增加母胎界面促炎细胞因子的产生,并过早激活分娩机制。尽管经过多年研究,仍没有广泛有效的预防早产策略,大多数治疗方法都是针对抑制子宫肌层收缩和改善新生儿结局。然而,近期关于孕激素和白细胞介素-10(IL-10)的研究在随机临床试验和动物研究中显示出前景。此外,将Toll样受体鉴定为炎症的上游介质,可能为预防这种常见的妊娠并发症提供替代治疗靶点。