ReviewNeonatology2013
Paneth cells and necrotizing enterocolitis: a novel hypothesis for disease pathogenesis.
Review in Neonatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
59 citing papers in PubMed, 96 citations in OpenAlex.
- Probiotic administration in congenital heart disease: a pilot study.Journal of perinatology : official journal of the California Perinatal Association · 2013Trial
- Nutritional management at 22-23 weeks gestational age: evidence and knowledge gaps.Pediatric research · 2026Review
- The gut-brain ConNECtion: exploring the developmental impact of necrotizing enterocolitis on the neonatal brain.Pediatric research · 2026Review
- Targeted immune response gene expression profiles linked with necrosis and mortality in preterm infants with surgical necrotizing enterocolitis.World journal of pediatric surgery · 2026Article
- Temporal dynamics of gut microbiota and virome in preterm infants: insights from longitudinal metagenomic analysis.Frontiers in cellular and infection microbiology · 2026Article
- Oxidative Stress in Neonatal Disease: Established Organ Injury and Emerging Evidence for Skeletal Involvement.Oxidative medicine and cellular longevity · 2026Review
- Attenuating Neurotoxicity Through Fecal Microbiota Transplant: Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Probiotics and the Risk of Infection.Clinics in perinatology · 2025Review
- Oxidative stress in pediatric diseases associated with the origin of life and growth and development.Frontiers in cell and developmental biology · 2025Review
- Paneth cell ontogeny in term and preterm ovine models.Frontiers in veterinary science · 2024Article
- Factors Influencing Neonatal Gut Microbiome and Health with a Focus on Necrotizing Enterocolitis.Microorganisms · 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
- Microbiota from Preterm Infants Who Develop Necrotizing Enterocolitis Drives the Neurodevelopment Impairment in a Humanized Mouse Model.Microorganisms · 2023Article
- Paneth cell development in the neonatal gut: pathway regulation, development, and relevance to necrotizing enterocolitis.Frontiers in cell and developmental biology · 2023Review
- Multifaceted involvements of Paneth cells in various diseases within intestine and systemically.Frontiers in immunology · 2023Review
- State-of-the-art review and update ofFrontiers in pediatrics · 2023Review
- Antimicrobial Peptides in Early-Life Host Defense, Perinatal Infections, and Necrotizing Enterocolitis-An Update.Journal of clinical medicine · 2022Review
- Intestinal epithelium in early life.Mucosal immunology · 2022Review
- Screening for modulators of the cellular composition of gut epithelia via organoid models of intestinal stem cell differentiation.Nature biomedical engineering · 2022Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Current models of necrotizing enterocolitis (NEC) propose that intraluminal microbes destroy intestinal mucosa and activate an inflammatory cascade that ends in necrosis. We suggest an alternate hypothesis wherein NEC is caused by injury to Paneth cells (PCs) in the intestinal crypts. PCs are specialized epithelia that protect intestinal stem cells from pathogens, stimulate stem cell differentiation, shape the intestinal microbiota, and assist in repairing the gut. Our novel model of NEC uses neonatal mice and ablates PCs followed by enteral infection. We contrast this model with other animal examples of NEC and the clinical disease. Selective destruction of PCs using dithizone likely releases tumor necrosis factor-α and other inflammatory mediators. We propose that this event produces inflammation in the submucosa, generates platelet-activating factor, and induces a coagulopathy. The role of PCs in NEC is consistent with the onset of disease in preterm infants after a period of PC-related maturation, the central role of PCs in crypt-related homeostasis, the anatomic location of pneumatosis intestinalis close to the crypts, and the proximity of PCs to occluded blood vessels that cause coagulation necrosis of the intestinal villi. We offer this hypothesis to promote new thoughts about how NEC occurs and its potential prevention.
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What OpenQuestion holds
Registered trials
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.