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Related Experiment Video

Updated: Jun 24, 2026

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Published on: July 28, 2023

Current concepts regarding the pathogenesis of necrotizing enterocolitis.

Mikael Petrosyan¹, Yigit S Guner, Monica Williams

¹Childrens Hospital Los Angeles, Keck School of Medicine, University of Southern California, 4650 Sunset Blvd, Mailstop #72, Los Angeles, CA 90027, USA.

Pediatric Surgery International

|March 21, 2009

Summary

Necrotizing enterocolitis (NEC), a severe intestinal disease in premature infants, lacks clear causes and effective treatments. Research into gut barrier failure mechanisms may offer new diagnostic and therapeutic strategies for this condition.

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A Novel Human Epithelial Enteroid Model of Necrotizing Enterocolitis

A Novel Human Epithelial Enteroid Model of Necrotizing Enterocolitis

Published on: April 10, 2019

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Last Updated: Jun 24, 2026

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Published on: July 28, 2023

A Novel Human Epithelial Enteroid Model of Necrotizing Enterocolitis

A Novel Human Epithelial Enteroid Model of Necrotizing Enterocolitis

Published on: April 10, 2019

Area of Science:

Neonatology
Gastroenterology
Pathophysiology

Background:

Necrotizing enterocolitis (NEC) is a critical gastrointestinal disease primarily affecting premature neonates.
Mortality rates for NEC have remained stagnant for decades, highlighting an urgent need for improved understanding and interventions.
The exact causes of NEC are unknown, but risk factors include gut bacteria, formula feeding, and perinatal stress, leading to epithelial destruction and gut barrier failure.

Purpose of the Study:

To explore the molecular and cellular mechanisms underlying gut barrier failure in NEC.
To investigate the role of endogenous mediators in NEC pathogenesis.
To enhance understanding of gut structural integrity and epithelial damage in NEC.

Main Methods:

Review of recent studies on NEC pathogenesis.
Analysis of the structural architecture of the gut barrier.
Examination of cellular mechanisms of gut epithelial damage.

Main Results:

Endogenous mediators like prostanoids, cyclooxygenases, and nitric oxide may contribute to gut barrier dysfunction in NEC.
Understanding the gut barrier's structural and cellular components is crucial for NEC research.

Conclusions:

Further research into the gut barrier's structure and cellular damage mechanisms is essential for developing novel diagnostic, prophylactic, and therapeutic strategies for NEC.
Elucidating NEC pathogenesis is critical for improving outcomes in premature infants.