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Updated: Aug 23, 2026

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Placental inflammation
1Case Western Reserve University and Department of Pathology, University Hospitals of Cleveland, 11100 Euclid Avenue, Cleveland, OH 44122, USA. raymond.redline@uhhs.com
Placental inflammatory disorders represent a diverse and important category of pathological processes leading to fetal and neonatal morbidity and mortality. These processes can be divided into two broad subcategories, those caused by micro-organisms and those caused by host immune responses to non-replicating antigens. The mechanisms by which these inflammatory processes cause death and disability are diverse and can be separated into four distinct classes: placental damage with loss of function, induction of premature labour and subsequent preterm birth, release of inflammatory mediators leading to fetal organ damage and transplacental infection of the fetus. Each specific inflammatory process can be modulated by properties of the specific organism, the route and timing of infection and variations in the host's genetic background and immune responsiveness. All of these factors combine to produce specific patterns of placental pathology that can be used to guide treatment, predict complications and explain adverse outcome.
Placental inflammatory disorders represent a diverse and important category of pathological processes leading to fetal and neonatal morbidity and mortality. These processes can be divided into two broad subcategories, those caused by micro-organisms and those caused by host immune responses to non-replicating antigens. The mechanisms by which these inflammatory processes cause death and disability are diverse and can be separated into four distinct classes: placental damage with loss of function, induction of premature labour and subsequent preterm birth, release of inflammatory mediators leading to fetal organ damage and transplacental infection of the fetus. Each specific inflammatory process can be modulated by properties of the specific organism, the route and timing of infection and variations in the host's genetic background and immune responsiveness. All of these factors combine to produce specific patterns of placental pathology that can be used to guide treatment, predict complications and explain adverse outcome.
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