ArticleDisease models & mechanisms2012
Paneth cell ablation in the presence of Klebsiella pneumoniae induces necrotizing enterocolitis (NEC)-like injury in the small intestine of immature mice.
Article in Disease models & mechanisms, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 103 citations in OpenAlex.
- Disruption of bile acid homeostasis potentiates Paneth cell ablation by activating the intestinal Farnesoid X receptor in necrotizing enterocolitis.NPJ biofilms and microbiomes · 2026Article
- Pathogenesis of necrotizing enterocolitis: mechanisms and mediators.World journal of pediatric surgery · 2026Review
- Molecular and Chromatin Accessibility Programs Underlying Epithelial Injury and Impaired Regeneration in Neonatal Necrotizing Enterocolitis.Cellular and molecular gastroenterology and hepatology · 2026Article
- Probiotics and the Risk of Infection.Clinics in perinatology · 2025Review
- Necrotizing enterocolitis causes increased ileal goblet cell loss inbioRxiv : the preprint server for biology · 2025Article
- FXR deletion attenuates intestinal barrier dysfunction in murine acute intestinal inflammation.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Endogenous Hyaluronan Promotes Intestinal Homeostasis and Protects against Murine Necrotizing Enterocolitis.Cells · 2024Article
- Host defense peptides human β defensin 2 and LL-37 ameliorate murine necrotizing enterocolitis.iScience · 2024Article
- Paneth cell ontogeny in term and preterm ovine models.Frontiers in veterinary science · 2024Article
- Immunological aspects of necrotizing enterocolitis models: a review.Frontiers in immunology · 2024Review
- Applying the bronchopulmonary dysplasia framework to necrotizing enterocolitis.Frontiers in pediatrics · 2024Article
- Pouchitis Is Associated with Paneth Cell Dysfunction and Ameliorated by Exogenous Lysosome in a Rat Model Undergoing Ileal Pouch Anal Anastomosis.Microorganisms · 2023Article
- Paneth cells in farm animals: current status and future direction.Journal of animal science and biotechnology · 2023Review
- Impact of neonatal nutrition on necrotizing enterocolitis.Seminars in pediatric surgery · 2023Review
- Paneth cell proteins DEFA6 and GUCA2A as tissue markers in necrotizing enterocolitis.European journal of pediatrics · 2023Article
- Development of the Neonatal Intestinal Barrier, Microbiome, and Susceptibility to NEC.Microorganisms · 2023Review
- Models of necrotizing enterocolitis.Seminars in perinatology · 2023Review
- State-of-the-art review and update ofFrontiers in pediatrics · 2023Review
- Multifaceted involvements of Paneth cells in various diseases within intestine and systemically.Frontiers in immunology · 2023Review
- Clinical and histopathological correlates of intestinal repair in preterm infants following surgical necrotizing enterocolitis.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2022Article
27 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Necrotizing enterocolitis (NEC) is a leading cause of morbidity and mortality in premature infants. During NEC pathogenesis, bacteria are able to penetrate innate immune defenses and invade the intestinal epithelial layer, causing subsequent inflammation and tissue necrosis. Normally, Paneth cells appear in the intestinal crypts during the first trimester of human pregnancy. Paneth cells constitute a major component of the innate immune system by producing multiple antimicrobial peptides and proinflammatory mediators. To better understand the possible role of Paneth cell disruption in NEC, we quantified the number of Paneth cells present in infants with NEC and found that they were significantly decreased compared with age-matched controls. We were able to model this loss in the intestine of postnatal day (P)14-P16 (immature) mice by treating them with the zinc chelator dithizone. Intestines from dithizone-treated animals retained approximately half the number of Paneth cells compared with controls. Furthermore, by combining dithizone treatment with exposure to Klebsiella pneumoniae, we were able to induce intestinal injury and inflammatory induction that resembles human NEC. Additionally, this novel Paneth cell ablation model produces NEC-like pathology that is consistent with other currently used animal models, but this technique is simpler to use, can be used in older animals that have been dam fed, and represents a novel line of investigation to study NEC pathogenesis and treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.