Amniotic fluid infection
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The chorion is composed of a reticular layer, basement membrane, and trophoblasts. The amnion is a fetal tissue comprising a layer of epithelial cells and underlying mesenchymal cells, and an extracellular matrix and collagen that has a high tensile strength. The amniotic sac is composed of maternal (decidua) and fetal components (chorion and amniotic membranes) which surround the fetus and represent one site of maternal/fetal immune interaction. Intraamniotic infection is an infection with resultant inflammation of any combination of the amniotic fluid (AF), placenta, fetus, fetal membranes, or decidua. Although sterile inflammation ( 3, 4), environmental pollutants ( 5– 7), cigarette smoke ( 8, 9), and other toxicants play an important role in the pathogenesis of IUI, these considerations are beyond the scope of this review. In particular, we review how inflammation is propagated in different tissue compartments at the maternal-fetal interface, the role of resident cells interacting with immune cells at the interface, the role of inflammatory mediators, and how host-microbe interactions affect pathology. In this paper, we explore the current knowledge of the mechanisms of IUI. Prematurity, which affects nearly 10% of pregnancies world-wide, is the most significant cause of perinatal mortality or morbidity ( 2).
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Intrauterine infection or inflammation (IUI), also known as chorioamnionitis, is responsible for ~40% of preterm labor cases ( 1). Lastly, we will discuss how infectious agents can break the maternal tolerance of fetal allograft during pregnancy and highlight the novel future therapeutic approaches.
![amniotic fluid infection amniotic fluid infection](https://facty.mblycdn.com/uploads/fh/2019/03/185086753-1024x855.jpg)
We will provide an overview of the knowledge gleaned from different animal models of acute chorioamnionitis and the role of different immune cells in different maternal-fetal compartments. Although less common, microorganisms invading the maternal-fetal interface via hematogenous route (e.g., Zika virus, Cytomegalovirus, and Listeria) can cause placental villitis and severe fetal inflammation and injury. Furthermore, recent vaginal microbiome studies suggest that there is a link between vaginal dysbiosis, vaginal inflammation, and ascending infection. Most commonly, acute chorioamnionitis is a result of ascending infection with relatively low-virulence organisms such as the Ureaplasma species. In this review, we will discuss current understanding of the pathogenesis, immunobiology, and mechanisms of this condition. It is a relatively common complication of pregnancy and can have devastating consequences including preterm labor, maternal infections, fetal infection/inflammation, fetal lung, brain, and gastrointestinal tract injury. Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, United StatesĪcute chorioamnionitis is characterized by neutrophilic infiltration and inflammation at the maternal fetal interface.Monica Cappelletti †, Pietro Presicce † and Suhas G.