早产是世界范围内一个普遍存在的现象，影响着5%-18%的孕妇，而且是新生儿死亡的最主要的原因。其致病机制的复杂性也决定了预防和治疗早产成为了生殖健康领域中一个长期而严峻的挑战，且由于缺少合适的动物模型，其致病机制仍知之甚少。利用p53子宫特异性敲除老鼠模拟人类早产过程，我们发现感染可以同时诱导母体蜕膜中的促炎症反应和抗炎症反应过程，这一过程的失衡是早产的一个重要原因，且在这个过程中蜕膜的p53在抗炎症过程中发挥着重要的作用，进一步的研究表明p53通过Stat3参与对抗炎症因子IL10的转录水平和表观水平的调控，在自发性早产和炎症诱导的早产过程中发挥重要。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 affects 5%-18% pregnant women and significantly accounts for neonatal morbidity and mortality. Due to the complex nature of the disease, preventing and curing PTB has proven difficult and to be a long-term challenge in reproductive health. Due to the lack of suitable animal for studying preterm birth, the mechanism is still unclear. Utilizing p53 uterine specific knockout mice to mimic human preterm birth, we found that infection will induce both pro-inflammation and anti-inflammation at the same time. The imbalance of this process will cause preterm birth. Further study suggested that p53 participate in anti-inflammation by regulating Stat3-IL10 at transcription and epigenetic level and play an important in spontaneous preterm birth and infection induced preterm birth. The results of this study will benefit for effectively developing novel therapeutic strategies for this multifaceted disease and will also alleviate the national-wide clinical, social and economic burden caused by this disorder.