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Related Experiment Video

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Author Spotlight: Enhancing Understanding and Treatment Strategies with the NEC-on-a-Chip Model
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Intestinal barrier dysfunction in human necrotizing enterocolitis.

Sarah A Moore1, Prashant Nighot2, Cynthia Reyes1

  • 1Department of Surgery, University of New Mexico, MSC10 5610 1 UNM, Albuquerque, NM 87131.

Journal of Pediatric Surgery
|October 11, 2016
PubMed
Summary
This summary is machine-generated.

Necrotizing enterocolitis (NEC) in infants involves increased intestinal permeability. This study found decreased occludin and increased myosin light chain kinase (MLCK) in NEC tissues, confirming barrier dysfunction.

Keywords:
Intestinal barrier functionNecrotizing enterocolitisOccludinTight junction

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Area of Science:

  • Neonatal research
  • Gastrointestinal physiology
  • Molecular biology

Background:

  • Intestinal barrier dysfunction is suspected in necrotizing enterocolitis (NEC).
  • Direct measurement of intestinal permeability in human NEC has been lacking.

Purpose of the Study:

  • To directly measure intestinal permeability in human NEC.
  • To investigate the molecular mechanisms underlying NEC-related intestinal barrier dysfunction.

Main Methods:

  • Small intestinal tissue samples from infants undergoing surgery were analyzed.
  • Ussing chamber technique was used to measure transepithelial resistance (TER) and mannitol flux.
  • Reverse transcription-polymerase chain reaction (RT-PCR) assessed mRNA expression of tight junction proteins (occludin) and myosin light chain kinase (MLCK).

Main Results:

  • Infant intestinal tissue with NEC exhibited significantly increased permeability (lower TER, higher mannitol flux) compared to controls.
  • NEC tissues showed a significant decrease in occludin mRNA expression.
  • Increased mRNA expression of myosin light chain kinase (MLCK) was observed in NEC specimens.

Conclusions:

  • Human NEC is characterized by increased intestinal permeability, even in macroscopically healthy areas.
  • Reduced occludin and elevated MLCK expression contribute to the intestinal barrier defect in NEC.