早产是一个多因素导致的综合症，是新生儿和幼儿死亡的最主要的原因，也是出生缺陷和新生儿疾病的首要病因，但是迄今为止，由于缺少合适的动物模型，早产的具体的分子机制还不是很清楚。本课题从蜕膜的角度出发，发现蜕膜中的基质细胞和内皮细胞有较高的TLR4表达，且进一步的利用基质细胞和内皮细胞条件性敲除小鼠发现，内皮细胞在炎症信号的传导过程中发挥着至关重要的作用。内皮细胞的TLR4在与LPS结合之后可以诱导NFkB的核转移，从而诱导Il6和Cox2在内皮细胞的表达，并进一步诱导Stat3在内皮细胞周围的基质细胞中磷酸化。Stat3通过诱导抗炎症因子IL10的表达以拮抗LPS诱导的炎症反应。通过注射IL10的重组蛋白，我们发现LPS诱导的早产得到了有效的缓解。因此，本研究成果将对制定及时有效的人工干预策略有着十分重要的指示性作用，而且可以缓解由于早产带来的一系列的全国性的社会问题和经济负担。

Preterm birth is a complex symptom originating from multiple reasons and significantly accounts for neonatal morbidity and mortality. The underlying mechanism remains enigmatic due to lack of suitable mouse model. Based on the critical role of decidua in preterm birth, we provide evidence that TLR4 is remarkably expressed in decidual stroma and endothelium. Using stromal and endothelial specific knockout mice model, we propose that endothelium is indispensable for inflammation induced preterm birth. After binding with TLR4, LPS stimulates the nuclear translocation of NFkB and induces the expression of IL6 and Cox2 in endothelial cells, then increases the phosphorylation of Stat3 in the stromal cells around the endothelium cells. The induced IL10 by Stat3 plays an important role in combating LPS induced preterm birth. By injection of recombinant IL10, the preterm birth induced by LPS is notably reduced. The results of this study will provide important information for clinical preterm birth interfere and will also alleviate the national-wide social- and economic- burden caused by this disorder.