ArticlePediatric research2023
Butyrate induces development-dependent necrotizing enterocolitis-like intestinal epithelial injury via necroptosis.
Article in Pediatric research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- NEC-Associated Bronchopulmonary Dysplasia and the Gut-Lung Axis in Preterm Infants.American journal of perinatology · 2026Review
- Short-chain fatty acids-a key link between the gut microbiome and T-lymphocytes in neonates?Pediatric research · 2026Review
- Sodium butyrate protects against necrotizing enterocolitis through a mechanism involving YB-1-dependent regulation of intestinal epithelial apoptosis.Scientific reports · 2026Article
- Gut microbiota and SCFA signatures in predicting postoperative infection sites in neurocritical care patients.Frontiers in microbiology · 2026Article
- IL-27Ra promotes the progression of neonatal necrotizing enterocolitis.Scientific reports · 2025Article
- Identification of potential necroinflammation-associated necroptosis-related biomarkers in necrotizing enterocolitis based on bioinformatics analysis and machine learning.Translational pediatrics · 2025Article
- The role of fecal short-chain fatty acids in neonatal necrotizing enterocolitis.Translational pediatrics · 2025Article
- Probiotics and the Risk of Infection.Clinics in perinatology · 2025Review
- Sodium Butyrate Inhibits Necroptosis by Regulating MLKL via E2F1 in Intestinal Epithelial Cells of Liver Cirrhosis.Journal of clinical and translational hepatology · 2025Article
- Sodium formate induces development-dependent intestinal epithelial injury via necroptosis and apoptosis.Redox report : communications in free radical research · 2024Article
- Vitamin E and GPX4 cooperatively protect treg cells from ferroptosis and alleviate intestinal inflammatory damage in necrotizing enterocolitis.Redox biology · 2024Article
- Receptor-interacting protein kinase-3 (RIPK3): a new biomarker for necrotising enterocolitis in preterm infants.Pediatric surgery international · 2024Article
- The Function of Necroptosis and Its Treatment Target in IBD.Mediators of inflammation · 2024Review
- The Impact of Stress, Microbial Dysbiosis, and Inflammation on Necrotizing Enterocolitis.Microorganisms · 2023Review
- Gut Microbiome-Brain Axis as an Explanation for the Risk of Poor Neurodevelopment Outcome in Preterm Infants with Necrotizing Enterocolitis.Microorganisms · 2023Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe accumulation of short-chain fatty acids (SCFAs) from bacterial fermentation may adversely affect the under-developed gut as observed in premature newborns at risk for necrotizing enterocolitis (NEC). This study explores the mechanism by which specific SCFA fermentation products may injure the premature newborn intestine mucosa leading to NEC-like intestinal cell injury.
methodsIntraluminal injections of sodium butyrate were administered to 14- and 28-day-old mice, whose small intestine and stool were harvested for analysis. Human intestinal epithelial stem cells (hIESCs) and differentiated enterocytes from preterm and term infants were treated with sodium butyrate at varying concentrations. Necrosulfonamide (NSA) and necrostatin-1 (Nec-1) were used to determine the protective effects of necroptosis inhibitors on butyrate-induced cell injury.
resultsThe more severe intestinal epithelial injury was observed in younger mice upon exposure to butyrate (p = 0.02). Enterocytes from preterm newborns demonstrated a significant increase in sensitivity to butyrate-induced cell injury compared to term newborn enterocytes (p = 0.068, hIESCs; p = 0.038, differentiated cells). NSA and Nec-1 significantly inhibited the cell death induced by butyrate.
conclusionsButyrate induces developmental stage-dependent intestinal injury that resembles NEC. A primary mechanism of cell injury in NEC is necroptosis. Necroptosis inhibition may represent a potential preventive or therapeutic strategy for NEC. IMPACT: Butyrate induces developmental stage-dependent intestinal injury that resembles NEC. A primary mechanism of cell injury caused by butyrate in NEC is necroptosis. Necroptosis inhibitors proved effective at significantly ameliorating the enteral toxicity of butyrate and thereby suggest a novel mechanism and approach to the prevention and treatment of NEC in premature newborns.
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