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Related Experiment Video

Updated: Apr 12, 2026

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
08:50

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

4.4K

An animal model for chorioamnionitis at term.

Valeria Dell'Ovo1, Jason Rosenzweig2, Irina Burd2

  • 1Department of Obstetrics and Gynecology, Center for Neural Repair and Rehabilitation, Shriners Hospitals Pediatric Research Center and Department of Obstetrics & Gynecology, Temple University School of Medicine, Philadelphia, PA.

American Journal of Obstetrics and Gynecology
|May 17, 2015
PubMed
Summary
This summary is machine-generated.

Maternal inflammation in late pregnancy can cause fetal brain injury. This study found a 4-hour window after maternal inflammation for potential therapeutic intervention to protect the developing fetal brain.

Keywords:
brain injurycerebral palsychorioamnionitis

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Area of Science:

  • Perinatal Medicine
  • Neuroscience
  • Toxicology

Background:

  • Intrapartum inflammation is linked to adverse neurologic outcomes in newborns.
  • Developing effective animal models is crucial for understanding maternal-fetal inflammatory responses.

Purpose of the Study:

  • To establish a rat model of intrapartum inflammation at term.
  • To investigate the impact of maternal inflammation on fetal brain development and inflammatory markers.

Main Methods:

  • Term-pregnant Sprague Dawley rats received intraperitoneal lipopolysaccharide (LPS).
  • Maternal and fetal outcomes, including plasma interleukin-6 (IL-6) and brain IL-6 expression, were measured.
  • Neuronal morphologic condition was assessed in primary cortical cell cultures using automated Sholl analysis.

Main Results:

  • Maternal IL-6 peaked rapidly post-LPS, with some persistence at higher doses.
  • Fetal brain IL-6 RNA and protein expression significantly increased 6 hours after LPS exposure.
  • Exposure to maternal inflammation reduced fetal cortical neuron neurite number and length in a dose-dependent manner.

Conclusions:

  • Systemic maternal inflammation induces fetal brain injury.
  • Fetal brain inflammation follows maternal stimulus, indicating a potential therapeutic window.
  • This model provides insights into the mechanisms of fetal neuroinflammation and injury.