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Updated: May 14, 2026
09:11
In Vitro Apical-Out Enteroid Model of Necrotizing Enterocolitis
Published on: June 8, 2022
Inflammatory signaling in necrotizing enterocolitis.
1Division of Neonatology, Department of Pediatrics, Children's Hospital of Chicago Research Center, Ann and Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, 225 East Chicago Avenue, Box 45, Chicago, IL 60611-2605, USA. isabelledp@northwestern.edu
Clinics in Perinatology
|February 19, 2013
Summary
Necrotizing enterocolitis (NEC) pathogenesis is complex. Animal models reveal inflammatory mediators play a key role in early NEC development, leading to a unifying hypothesis.
Area of Science:
- Neonatal research
- Gastroenterology
- Inflammation
Background:
- Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease in neonates.
- Understanding NEC pathogenesis is challenging due to late-stage tissue availability.
- Animal models are crucial for studying early NEC development.
Purpose of the Study:
- To review evidence on inflammatory mediators in NEC pathogenesis.
- To propose a unifying hypothesis for early NEC development.
Main Methods:
- Literature review of studies on NEC pathogenesis.
- Analysis of data from animal models of NEC.
- Synthesis of evidence regarding inflammatory mediators.
Main Results:
- Inflammatory mediators are implicated in NEC development.
- Animal models have identified key roles for specific inflammatory pathways.
- Evidence supports a complex inflammatory network in NEC.
Conclusions:
- Inflammatory mediators are central to NEC pathogenesis.
- A unifying hypothesis integrating inflammatory roles in early NEC is proposed.
- Further research using animal models can elucidate NEC mechanisms.
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