ArticleThe Journal of surgical research2023
Apical-Out Enteroids as an Innovative Model for Necrotizing Enterocolitis.
Article in The Journal of surgical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Optimising the induction of inflammation within preterm infant-derived intestinal epithelial organoids.Npj gut and liver · 2026Article
- Persistent Post-Recovery Hyperinflammation of Necrotizing Enterocolitis Is Ameliorated by 5-ASA Treatment.Surgical infections · 2025Article
- Molecular mechanisms of co-infections.EMBO reports · 2025Review
- The Role of GPX Enzymes, Lipid Profiles, and Iron Accumulation in Necrotizing Enterocolitis.International journal of molecular sciences · 2025Article
- Crosstalk Within the Intestinal Epithelium: Aspects of Intestinal Absorption, Homeostasis, and Immunity.Biomedicines · 2024Review
- Age-Specific ADME Gene Expression in Infant Intestinal Enteroids.Molecular pharmaceutics · 2024Article
- Neonatal enteroids absorb extracellular vesicles from human milk-fed infant digestive fluid.Journal of extracellular vesicles · 2024Article
- Immunological aspects of necrotizing enterocolitis models: a review.Frontiers in immunology · 2024Review
- Despite Recovery from Necrotizing Enterocolitis Infants Retain a Hyperinflammatory Response to Injury.Journal of inflammation research · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
introductionNecrotizing enterocolitis (NEC) is a gastrointestinal disease of premature neonates. We previously validated a NEC enteroid model derived from human infant intestinal tissue. Typical enteroid configuration is basolateral-out (BO) without direct access to the luminal (apical) surface. Apical access is necessary to allow physiologic comparison of pathogen interaction with the intestinal epithelial barrier. We hypothesize that apical-out (AO) enteroids will provide a relevant NEC model to study this relationship.
methodsFollowing the institutional review board approval (#11610-11611), neonatal intestinal tissue was collected from surgical specimens. Stem cells were collected; enteroids were generated and grown to maturity in BO conformation then everted to AO. Enteroids were untreated or treated for 24 h with 100 μg/mL lipopolysaccharide and hypoxia. Protein and gene expression were analyzed for inflammatory markers, tight junction (TJ) proteins and permeability characteristic of NEC.
resultsApical TJ protein zonula occludens-1 and basolateral protein β-catenin immunofluorescence confirmed AO configuration. Treated AO enteroids had significantly increased messenger RNA (P = 0.001) and protein levels (P < 0.0001) of tumor necrosis factor-α compared to controls. Corrected total cell fluorescence of toll-like receptor 4 was significantly increased in treated AO enteroids compared to control (P = 0.002). Occludin was found to have significantly decreased messenger RNA in treated AO enteroids (P = 0.003). Expression of other TJ proteins claudins-1, -4 and zonula occludens-1 was significantly decreased in treated AO enteroids (P < 0.05).
conclusionsAO enteroids present an innovative model for NEC with increased inflammation and gut barrier restructuring. This model allows for a biologically relevant investigation of the interaction between the pathogen and the intestinal epithelial barrier in NEC.
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