Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus.
Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus.
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DOI：
10.1007/s00281-020-00807-y
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发表时间：
2020-08
影响因子：
9
通讯作者：
Arck PC
中科院分区：
文献类型：
--
作者：
Green ES;Arck PC
早产（PTB）使全球5-18%的妊娠复杂化，是孕产妇和胎儿发病率和死亡率的主要原因。大多数PTB是自发性和特发性的，原因很大程度上不明确。为了增加对PTB的理解，近年来的许多研究都集中在使用动物模型来概括PTB的病理生理学。母体免疫适应功能障碍与一系列妊娠病理学有关，包括PTB。来自小鼠模型以及人类研究的大量证据现在可用于支持PTB是由胎儿-母体耐受性的破坏以及过度的过早炎症沿着引起的。在这篇综述中，我们研究了目前的知识，胎儿和母体系统之间的双向通信及其在PTB的免疫发病机制中的作用。这些最新的见解显着推进我们对PTB的发病机制的理解，这是至关重要的，最终设计更有效的策略，早期预测和随后的预防PTB。
Preterm birth (PTB) complicates 5–18% of pregnancies globally and is a leading cause of maternal and fetal morbidity and mortality. Most PTB is spontaneous and idiopathic, with largely undefined causes. To increase understanding of PTB, much research in recent years has focused on using animal models to recapitulate the pathophysiology of PTB. Dysfunctions of maternal immune adaptations have been implicated in a range of pregnancy pathologies, including PTB. A wealth of evidence arising from mouse models as well as human studies is now available to support that PTB results from a breakdown in fetal-maternal tolerance, along with excessive, premature inflammation. In this review, we examine the current knowledge of the bidirectional communication between fetal and maternal systems and its role in the immunopathogenesis of PTB. These recent insights significantly advance our understanding of the pathogenesis of PTB, which is essential to ultimately designing more effective strategies for early prediction and subsequent prevention of PTB.
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