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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
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Heterogeneity in inflammatory responses to endotoxin at the fetomaternal interface
Vineeth Mahajan1, Madhuri Tatiparthy1, Tilu Jain Thomas1
1Division of Basic Science and Translational Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, TX, United States.
Journal of Immunology (Baltimore, Md. : 1950)
|March 18, 2026
Summary
Maternal decidual cells show heightened inflammatory responses to endotoxin, while fetal cells at the fetomaternal interface exhibit a muted reaction, suggesting a protective mechanism during pregnancy inflammation.
Area of Science:
- Immunology
- Reproductive Biology
- Cell Biology
Background:
- The fetomaternal interface (FMI) is crucial for immune tolerance during pregnancy.
- Intrauterine inflammation is a significant cause of adverse pregnancy outcomes like preterm birth.
- Cell-specific inflammatory responses at the FMI are not well understood.
Purpose of the Study:
- To investigate the differential inflammatory responses of fetal chorionic trophoblast cells (CTCs) and maternal decidual stromal cells (DECs) at the FMI upon exposure to lipopolysaccharide (LPS).
- To identify cell-specific regulatory pathways involved in these responses.
Main Methods:
- Primary human CTCs and DECs were isolated from term fetal membranes.
- Cells were treated with LPS (100 ng/mL) for 48 hours.
- Transcriptomic profiling, multiplex immunoassays, western blotting, and regulatory network analysis were performed.
Main Results:
- Maternal DECs displayed a strong inflammatory response to LPS, with increased proinflammatory chemokines and prostaglandin enzymes.
- Fetal CTCs showed an attenuated response, with induction of stress-associated genes and minimal inflammatory pathway activation.
- Distinct cell-type-specific regulatory hubs (STAT1, IRF7 in DECs; RELA, MYD88 in CTCs) were identified.
- DECs activated anti-inflammatory and pyroptosis pathways, largely absent in CTCs.
Conclusions:
- There is fundamental heterogeneity in inflammatory responses at the FMI, with maternal cells being more sensitive to LPS than fetal CTCs.
- These differential responses may serve to protect the fetus from excessive inflammation.
- Understanding these cell-specific responses is vital for comprehending pregnancy tolerance and identifying therapeutic targets for inflammation-associated complications.
