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Related Experiment Video

Updated: May 6, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

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Complement Modulation Mitigates Inflammation-Mediated Preterm Birth and Fetal Neural Inflammation.

Eliza R McElwee1, Devin Hatchell2, Mohammed Alshareef3

  • 1Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.

Cells
|July 25, 2025
PubMed
Summary

Complement inhibition targeting inflammation can prevent preterm birth. A novel inhibitor (CR2-Crry) reduced inflammation and improved delivery outcomes in an LPS-induced preterm birth model.

Keywords:
complement modulationcomplement systemfetal inflammationmaternal-fetal interfacepreterm birth

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Area of Science:

  • Reproductive biology
  • Immunology
  • Maternal-fetal medicine

Background:

  • Preterm birth is linked to maternal and fetal inflammation.
  • The complement system plays a role in this inflammatory response.

Purpose of the Study:

  • Investigate complement activation in an LPS-induced preterm birth model.
  • Evaluate a complement inhibitor (CR2-Crry) for therapeutic potential.

Main Methods:

  • Utilized an LPS inflammation-induced preterm birth model.
  • Administered LPS and a targeted complement inhibitor (CR2-Crry).
  • Analyzed complement activation products, inflammatory cytokines, and macrophage recruitment in maternal and fetal tissues.

Main Results:

  • Complement-mediated inflammation contributes to preterm delivery.
  • CR2-Crry treatment mitigated LPS-induced pathology and preterm birth.
  • Inhibition increased gestational age and pup viability, reducing inflammation.

Conclusions:

  • Targeted complement inhibition is a potential therapeutic strategy for preventing preterm birth.
  • Site-specific inhibition minimizes off-target effects.