Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus
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REVIEW
Pathogenesis of preterm birth: bidirectional inflammation in mother and fetus Ella Shana Green 1 & Petra Clara Arck 1 Received: 31 March 2020 / Accepted: 14 July 2020 # The Author(s) 2020
Abstract 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 fetalmaternal 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. Keywords Preterm birth . Labor . Mouse models . Regulatory T cells . Inflammatory signaling pathways . Microbiome . Fetal signals
Introduction Preterm birth (PTB), defined as birth before the 37th week of gestation, affects up to 15 million pregnancies each year globally [1]. Being born too soon can lead to neonatal death, but also a high risk for early-life infections and neurodevelopmental, cardiometabolic, and inflammatory disorders later in the life of surviving infants [2–6]. A current understanding of the complex pathogenesis of PTB is still poor, which also explains the limited availability of targeted and effective strategies for PTB prevention. Several risk factors for PTB are well recognized, such as twin pregnancies, chorioamnionitis, pre-existing maternal
This article is a contribution to the special issue on Preterm birth: Pathogenesis and clinical consequences revisited – Guest Editors: Anke Diemert and Petra Arck * Petra Clara Arck [email protected] 1
Department of Obstetrics and Fetal Medicine, Laboratory for Experimental Feto-Maternal Medicine, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20251 Hamburg, Germany
diseases, genetic factors, previous PTB, and uterine abnormalities [7–10]. However, a large proportion of PTBs have no identifiable cause. These spontaneous PTBs present as pathological inflammation, premature rupture of membranes (PROM), and onset of preterm labor. Interestingly, inflammation is also a key trigger of the physiological onset of labor at term [11]. Thus, the onset of inflammation seems to be a common denominator initiating term as well as preterm labor. Here, we comprehensively review why inflammation may be prematurely initiated in some pregnancies, which then leads to PTB.
A brief overview of maternal immune adaptation dur
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