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Related Experiment Video

Updated: Jun 12, 2025

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An anti-eCIRP strategy for necrotizing enterocolitis.

Colleen P Nofi1,2,3, Jose M Prince1,3, Mariana R Brewer4

  • 1Center for Immunology and Inflammation, the Feinstein Institutes for Medical Research, 350 Community Dr., Manhasset, NY, 11030, USA.

Molecular Medicine (Cambridge, Mass.)
|September 20, 2024
PubMed
Summary
This summary is machine-generated.

Extracellular cold-inducible RNA-binding protein (eCIRP) worsens necrotizing enterocolitis (NEC). Targeting eCIRP with MOP3 peptide significantly improves survival and reduces injury in a mouse model of NEC.

Keywords:
InflammationMFG-E8MOP3Necrotizing enterocolitiseCIRP

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Area of Science:

  • Neonatal research
  • Gastroenterology
  • Immunology

Background:

  • Necrotizing enterocolitis (NEC) is a severe neonatal gastrointestinal disease with high mortality.
  • Extracellular cold-inducible RNA-binding protein (eCIRP) is implicated in inflammation and tissue injury.
  • The role of eCIRP in NEC pathogenesis is currently unknown.

Purpose of the Study:

  • To investigate the role of eCIRP in NEC.
  • To evaluate the therapeutic potential of an eCIRP-scavenging peptide, MOP3, in NEC.

Main Methods:

  • Measured eCIRP levels in stool samples from neonates with and without NEC.
  • Utilized a murine model of NEC involving hypoxia, hypercaloric gavage, and LPS.
  • Assessed NEC severity, intestinal and lung injury, barrier dysfunction, and survival in wild-type and CIRP knockout mice, with and without MOP3 treatment.

Main Results:

  • Elevated eCIRP levels were found in NEC neonates.
  • CIRP knockout mice were significantly protected against NEC, showing reduced injury and inflammation, with 100% survival.
  • MOP3 treatment improved NEC survival to 80% and attenuated organ injury and inflammation.

Conclusions:

  • eCIRP exacerbates NEC pathogenesis, as evidenced by protection in CIRP-deficient mice.
  • MOP3, a novel therapeutic targeting eCIRP, shows promise in treating NEC.
  • eCIRP represents a relevant therapeutic target for human NEC.