Preterm birth and sustained inflammation: consequences for the neonate.

Preterm birth and sustained inflammation: consequences for the neonate.
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DOI:
10.1007/s00281-020-00803-2
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发表时间:
2020-08
影响因子:
9
通讯作者:
German Neonatal Network, German Center for Lung Research and Priming Immunity at the beginning of life (PRIMAL) Consortium
German Neonatal Network, German Center for Lung Research and Priming Immunity at the beginning of life (PRIMAL) Consortium
中科院分区:
医学1区
文献类型:
--
作者:
Humberg A;Fortmann I;Siller B;Kopp MV;Herting E;Göpel W;Härtel C;German Neonatal Network, German Center for Lung Research and Priming Immunity at the beginning of life (PRIMAL) Consortium

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几乎一半的早产是由胎儿-母体界面的炎症过程引起或触发的,导致早产或胎膜破裂,伴或不伴绒毛膜羊膜炎(“第一次炎症打击”)。早产儿的身体表面非常脆弱,器官系统不成熟。他们在出生后面临着急剧变化的抗原暴露,包括医院特有的微生物、人工设备、药物、营养抗原以及缺氧或高氧(“第二次炎症打击”)。这对于 28 周之前出生的极早产儿尤其重要,因为他们没有经历重要的“妊娠晚期”适应过程来耐受母体抗原和自身抗原。因此,免疫防御机制和免疫抑制(耐受性)之间微妙的共同调节(以允许微生物组的建立)经常受到干扰,而不是对宫外生活的平衡适应。因此,早产儿容易患败血症,但也容易患上几种可能导致持续炎症 (SI) 发作或持续的损伤性疾病。这对参与早产儿护理的临床医生来说是一个持续的挑战,因为 SI 被认为是早产儿死亡率和发病的重要中介因素。本综述将概述 (i) 炎症对早产短期后果的作用,以及 (ii) SI 对器官发育和长期结果的影响。
Almost half of all preterm births are caused or triggered by an inflammatory process at the feto-maternal interface resulting in preterm labor or rupture of membranes with or without chorioamnionitis (“first inflammatory hit”). Preterm babies have highly vulnerable body surfaces and immature organ systems. They are postnatally confronted with a drastically altered antigen exposure including hospital-specific microbes, artificial devices, drugs, nutritional antigens, and hypoxia or hyperoxia (“second inflammatory hit”). This is of particular importance to extremely preterm infants born before 28 weeks, as they have not experienced important “third-trimester” adaptation processes to tolerate maternal and self-antigens. Instead of a balanced adaptation to extrauterine life, the delicate co-regulation between immune defense mechanisms and immunosuppression (tolerance) to allow microbiome establishment is therefore often disturbed. Hence, preterm infants are predisposed to sepsis but also to several injurious conditions that can contribute to the onset or perpetuation of sustained inflammation (SI). This is a continuing challenge to clinicians involved in the care of preterm infants, as SI is regarded as a crucial mediator for mortality and the development of morbidities in preterm infants. This review will outline the (i) role of inflammation for short-term consequences of preterm birth and (ii) the effect of SI on organ development and long-term outcome.
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