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Related Experiment Video

Updated: May 31, 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

Chorioamnionitis - new ideas from experimental models.

Boris W Kramer1

  • 1Division of Neonatology, Department of Pediatrics, Maastricht University Medical Center, Maastricht, The Netherlands. b.kramer@mumc.nl

Neonatology
|June 25, 2011
PubMed
Summary
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Antenatal inflammation, like chorioamnionitis, can harm newborns. This study used sheep models to show lipopolysaccharide (LPS) and Ureaplasma infections cause organ damage and immune changes, highlighting the need for further research.

Area of Science:

  • Reproductive biology
  • Neonatal immunology
  • Fetal medicine

Background:

  • Antenatal inflammation is linked to adverse neonatal outcomes.
  • Microbial invasion of the amniotic cavity, known as chorioamnionitis, involves bacteria and viruses.
  • Causes, onset timing, and fetal responses in chorioamnionitis require further elucidation.

Purpose of the Study:

  • To investigate the effects of induced chorioamnionitis on fetal organ systems and systemic responses in a sheep model.
  • To explore the distinct impacts of lipopolysaccharide (LPS) and Ureaplasma species on fetal development and inflammation.
  • To identify potential therapeutic targets by understanding the mechanisms of inflammation and damage.

Main Methods:

  • Chorioamnionitis was induced in pregnant sheep via amniotic cavity injections of lipopolysaccharide (LPS) or Ureaplasma species.

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Last Updated: May 31, 2026

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
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  • Ultrasound guidance was employed for accurate injections.
  • Organ-specific and systemic effects were assessed following induced infections.
  • Main Results:

    • LPS-induced chorioamnionitis led to a cascade of organ injury, inflammation, and remodeling, with associated systemic effects.
    • Systemic effects of LPS exposure included immune suppression (cross-tolerance) to Toll-like receptor agonists.
    • Ureaplasma-induced chorioamnionitis resulted in time-dependent alterations in fetal lung structure.

    Conclusions:

    • Induced chorioamnionitis in a sheep model replicates key aspects of human disease, providing a valuable research platform.
    • Lipopolysaccharide and Ureaplasma infections elicit distinct inflammatory and structural responses in the fetus.
    • Further research into the mechanisms of inflammation, structural damage, and growth factor expression is crucial for developing therapeutic strategies.