ArticleFrontiers in immunology2025
Neutrophils aggravate inflammatory lesions in intestinal organoids from necrotizing enterocolitis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Sunflower oil-loaded lycopene protects intestinal barrier integrity following traumatic brain injury.Journal of molecular histology · 2026Article
- Identification and validation of a robust inflammation-related three-gene signature for the diagnosis of neonatal necrotizing enterocolitis via machine learning integration.Pediatric surgery international · 2026Article
- All roads lead to NF-κB: the NF-κB pathway as a major target for intestinal inflammatory disorders.Frontiers in immunology · 2026Review
- Stage-specific neutrophil states in neonatal injury: from antimicrobial deficiency to pro-resolution repair.Frontiers in immunology · 2026Review
- DNase1 reverses peribronchial inflammation in murine explants incubated with activated neutrophils.Frontiers in immunology · 2026Article
- The role of myeloid cells in the pathogenesis of necrotizing enterocolitis; a scoping review.Frontiers in pediatrics · 2026Review
- A Potentially TREMendous Treatment: TREM1 Inhibition as a Novel Therapy for Necrotizing Enterocolitis.Digestive diseases and sciences · 2025Article
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Authors and funding
11 authors.
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Abstract
Introduction: Necrotizing enterocolitis (NEC) is a leading cause of neonatal death and long-term morbidity, involving complex pathophysiology including prematurity, abnormal bacterial colonization, and ischemia-reperfusion injury, partially mediated by neutrophils. However, the limitations of current animal models hinder the development of targeted therapies for NEC. Thus, this study aimed to develop a human intestinal organoid model for NEC to investigate its pathophysiology, understand neutrophil involvement, and bridge animal and human research. Methods: Organoid cultures were established from human neonatal intestinal samples with NEC (n=7) and without gut inflammation (controls, n=7), treated with lipopolysaccharides (LPS), and/or cocultured with neutrophils. Flow cytometry quantified neutrophil survival (propidium iodide/Annexin-V), activation (CD11b/CD66b), and TLR-4 expression, as well as organoid TLR-4 expression and apoptosis markers. NEC status and neutrophil recruitment were analyzed using immunofluorescence. Results: After LPS administration, NEC organoids showed significantly increased TLR-4 expression, intestinal apoptosis markers, and NEC scores compared to controls, with more pronounced differences after neutrophil addition. Neutrophil activation markers were elevated when cocultured with both NEC and control organoids, but TLR-4 expression increased only with NEC organoids. Discussion: The findings suggest that epithelial cells from NEC patients have a heightened innate TLR-4 expression upon LPS stimulation, potentially contributing to NEC development. LPS stimulation resulted in more pronounced NEC-like lesions in NEC organoids, which were exacerbated by neutrophils. This model demonstrates that neutrophils might contribute to NEC manifestation and maintenance and that NEC organoids can reflect disease aspects, potentially aiding in the development of targeted therapies.
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