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Related Experiment Video

Updated: Sep 6, 2025

Testing Epithelial Permeability in Fetal Tissue-Derived Enteroids
07:51

Testing Epithelial Permeability in Fetal Tissue-Derived Enteroids

Published on: June 16, 2022

2.2K

Testing Epithelial Permeability in Fetal Tissue-Derived Enteroids.

Amelia Llerena1, Shaheda Urmi2, Jahanshah Amin3

  • 1Morsani College of Medicine, University of South Florida.

Journal of Visualized Experiments : Jove
|July 5, 2022
PubMed
Summary
This summary is machine-generated.

Human fetal enteroids model preterm infant intestinal injury. Lipopolysaccharide exposure increased enteroid permeability, supporting dysbiosis as a risk factor.

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Area of Science:

  • Gastroenterology
  • Developmental Biology
  • Microbiology

Background:

  • Human fetal tissue-derived enteroids offer a novel in vitro model for studying intestinal injuries in preterm infants.
  • Intestinal injuries in preterm infants lead to mucosal inflammation and increased permeability, which are difficult to assess directly in patients.
  • Enteroids mimic intestinal structure and function, enabling investigation of epithelial permeability and tight junction protein regulation.

Purpose of the Study:

  • To establish and characterize human fetal enteroids as a model for intestinal injury.
  • To investigate the role of lipopolysaccharide (LPS) in inducing epithelial permeability in enteroids.
  • To explore the contribution of gram-negative bacterial dysbiosis to intestinal injury mechanisms in preterm infants.

Main Methods:

  • Establishing enteroids from human fetal intestinal tissue.
  • Characterizing tight junction proteins using immunofluorescent imaging.
  • Quantifying paracellular permeability by microinjecting fluorescein-labeled dextran into enteroid lumens and measuring leakage.

Main Results:

  • Apical exposure to lipopolysaccharide (LPS) induced epithelial permeability in enteroids in a concentration-dependent manner.
  • Enteroid tight junction proteins were characterized, providing a basis for assessing permeability changes.
  • The model successfully demonstrated LPS-induced permeability, mimicking effects of gram-negative bacterial dysbiosis.

Conclusions:

  • Human fetal enteroids serve as a viable in vitro model for studying intestinal injuries in preterm infants.
  • Lipopolysaccharide exposure increases enteroid epithelial permeability, supporting its role in intestinal injury.
  • These findings suggest that gram-negative dominant dysbiosis is a significant contributor to intestinal injury mechanisms in preterm infants.