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Updated: May 18, 2026
06:51
Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
Published on: July 28, 2023
Paneth cells and necrotizing enterocolitis: a novel hypothesis for disease pathogenesis
Steven J McElroy1, Mark A Underwood, Michael P Sherman
1Division of Neonatology, Department of Pediatrics, University of Iowa, Iowa City, Iowa, USA.
Neonatology
|September 26, 2012
Summary
Necrotizing enterocolitis (NEC) may stem from Paneth cell injury, not just microbes. This new hypothesis suggests Paneth cell damage triggers inflammation and coagulopathy, offering novel prevention strategies for this infant disease.
Area of Science:
- Gastroenterology
- Neonatal Research
- Cell Biology
Background:
- Current necrotizing enterocolitis (NEC) models implicate intraluminal microbes in intestinal mucosal destruction and inflammation.
- Paneth cells (PCs) are crucial for intestinal homeostasis, protecting stem cells, modulating microbiota, and aiding repair.
Purpose of the Study:
- To propose an alternative hypothesis for NEC pathogenesis centered on Paneth cell injury.
- To investigate the role of Paneth cells in a novel mouse model of NEC.
Main Methods:
- Developed a novel NEC model in neonatal mice by ablating Paneth cells (PCs) using dithizone, followed by enteral infection.
- Compared this model with existing animal NEC models and clinical NEC observations.
Main Results:
- Selective PC ablation in mice may release inflammatory mediators like tumor necrosis factor-α.
- Proposed mechanism involves submucosal inflammation, platelet-activating factor generation, and coagulopathy following PC injury.
Conclusions:
- Paneth cell injury is a plausible alternative cause of NEC, aligning with disease onset in preterm infants and crypt-level pathology.
- This hypothesis provides a new framework for understanding NEC and exploring preventative measures.
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