Spontaneous preterm birth (PTB) and preterm pre-labor rupture of the membranes (pPROM) are major pregnancy complications. Although PTB and pPROM have common etiologies, they arise from distinct pathophysiologic pathways. Inflammation is a common underlying mechanism in both conditions. Balanced inflammation is required for fetoplacental growth; however, overwhelming inflammation (physiologic at term and pathologic at preterm) can lead to term and preterm parturition. A lack of effective strategies to control inflammation and reduce the risk of PTB and pPROM suggests that there are several modes of the generation of inflammation which may be dependent on the type of uterine tissue. The avascular fetal membrane (amniochorion), which provides structure, support, and protection to the intrauterine cavity, is one of the key contributors of inflammation. Localized membrane inflammation helps tissue remodeling during pregnancy. Two unique mechanisms that generate balanced inflammation are the progressive development of senescence (aging) and cyclic cellular transitions: epithelial to mesenchymal (EMT) and mesenchymal to epithelial (MET). The intrauterine build-up of oxidative stress at term or in response to risk factors (preterm) can accelerate senescence and promote a terminal state of EMT, resulting in the accumulation of inflammation. Inflammation degrades the matrix and destabilizes membrane function. Inflammatory mediators from damaged membranes are propagated via extracellular vesicles (EV) to maternal uterine tissues and transition quiescent maternal uterine tissues into an active state of labor. Membrane inflammation and its propagation are fetal signals that may promote parturition. This review summarizes the mechanisms of fetal membrane cellular senescence, transitions, and the generation of inflammation that contributes to term and preterm parturitions.

自发性早产 (PTB) 和早产胎膜早破 (pPROM) 是主要的妊娠并发症。尽管 PTB 和 pPROM 具有共同的病因，但它们起源于不同的病理生理途径。在这两种情况下，炎症都是一种常见的潜在机制。胎儿胎盘生长需要平衡炎症；然而，压倒性炎症（足月生理性炎症和早产病理性炎症）可导致足月和早产。缺乏有效的控制炎症和降低 PTB 和 pPROM 风险的策略表明存在多种炎症产生模式，这可能取决于子宫组织的类型。为宫腔提供结构、支撑和保护的无血管胎膜（羊膜绒毛膜）是炎症的关键因素之一。局部膜炎症有助于怀孕期间的组织重塑。产生平衡炎症的两种独特机制是衰老（老化）和循环细胞转变的进行性发展：上皮到间充质 (EMT) 和间充质到上皮 (MET)。足月或对危险因素（早产）的宫内氧化应激积累可加速衰老并促进 EMT 的终末状态，从而导致炎症的积累。炎症会降解基质并使膜功能不稳定。来自受损膜的炎症介质通过细胞外囊泡 (EV) 传播到母体子宫组织，并将静止的母体子宫组织转变为活跃的分娩状态。膜炎症及其传播是可能促进分娩的胎儿信号。