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Updated: Jun 23, 2026
A Novel Human Epithelial Enteroid Model of Necrotizing Enterocolitis
Published on: April 10, 2019
Epithelial functions of the residual bowel after surgery for necrotising enterocolitis in human infants
Maaike W Schaart1, Adrianus C J M de Bruijn, Deirdre M Bouwman
1Department of Pediatrics, Erasmus MC-Sophia Children's Hospital, The Netherlands.
Insights
Necrotising enterocolitis (NEC) in infants disrupts intestinal epithelial cell function and proliferation. Residual bowel shows impaired barrier defense due to goblet and Paneth cell loss, with marker expression normalizing after stoma closure.
Area of Science:
- Gastroenterology
- Pediatric Surgery
- Cell Biology
Background:
- Necrotising enterocolitis (NEC) is a critical condition in neonates requiring bowel resection.
- Limited data exists on the epithelial function of residual bowel after NEC surgery.
Purpose of the Study:
- To assess epithelial functions in intestinal resection margins from infants undergoing surgery for NEC.
- To evaluate changes at acute NEC and after stoma closure.
Main Methods:
- (Immuno)histochemical analysis of epithelial morphology, proliferation, and protein expression.
- Studied specific markers including lactase, glucose transporters, sucrase-isomaltase, intestinal fatty acid binding protein, mucin 2, trefoil factor 3, and lysozyme.
Main Results:
- NEC caused varied epithelial damage, increased proliferation, and down-regulation of specific enterocyte proteins.
- Goblet and Paneth cell numbers decreased, impacting mucin and lysozyme expression.
- Epithelial marker expression fully recovered by stoma closure.
Conclusions:
- Residual bowel after NEC resection exhibits an imbalanced epithelial proliferation and differentiation.
- Acute NEC impairs enterocyte-specific protein expression and reduces protective goblet and Paneth cells.
- These changes may compromise mucosal barrier and defense functions.
Objectives:
Information on epithelial functions of the residual small or colonic bowel after resection for necrotising enterocolitis (NEC) in human infants is scarce. Our aim is to evaluate epithelial functions in the intestinal resection margins of tissue obtained at bowel resection for acute NEC and consecutive stoma closure.
Materials And Methods:
Epithelial morphology, proliferation, and protein expression were (immuno)histochemically studied.
Results:
Acute NEC was associated with severe and mild epithelial damage varying from epithelial loss to fairly unaffected epithelium. Epithelial proliferation was increased both at acute NEC and at stoma closure. In acute NEC, lactase, glucose transporter-2 and -5 expression was down-regulated in severely affected epithelium, whereas sucrase-isomaltase and intestinal fatty acid binding protein expression was maintained. Goblet cells continued to express mucin 2 and trefoil factor 3, however, their numbers were decreased. Moreover, in acute NEC, Paneth cells were weakly lysozyme positive and were reduced in number. At stoma closure, expression of the above cell type-specific markers had completely been re-established.
Conclusions:
Residual bowel after resection for acute NEC shows a disturbed epithelial proliferation/differentiation balance. Acute NEC was associated with downregulation of distinct enterocyte-specific proteins. Because of goblet cell and Paneth cell loss in acute NEC, mucosal barrier, and defense functions may be impaired.
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