Intestinal alkaline phosphatase administration in newborns is protective of gut barrier function in a neonatal necrotizing enterocolitis rat model

J Pediatr Surg. 2012 Jun;47(6):1135-42. doi: 10.1016/j.jpedsurg.2012.03.018.

Abstract

Background: Previously, we have shown that supplementation of intestinal alkaline phosphatase (IAP) decreased severity of necrotizing enterocolitis (NEC)-associated intestinal injury. We hypothesized that IAP administration is protective of intestinal epithelial barrier function in a dose-dependent manner.

Methods: Control rat pups were vaginally delivered and breast-fed. Premature rats were divided into 4 groups: formula fed with lipopolysaccharide and hypoxia (NEC) or additional daily bovine IAP 40, 4, or 0.4 U/kg (NEC + IAP 40 U, IAP 4 U, or IAP 0.4 U).

Results: Necrotizing enterocolitis is associated with decreased IAP protein expression and activity. Supplemental IAP increases IAP activity in intestinal homogenates and decreased NEC injury score in a dose-dependent manner. Intestinal injury as measured by fluorescein isothiocyanate-dextran flux from ileal loops showed increased permeability vs control, but supplemental IAP reversed this. Tight junction proteins claudin-1, claudin-3, occludin, and zonula occludin 1 were elevated in the NEC and IAP-treated groups with differences in expression patterns. No differences in messenger RNA levels were observed on postinjury day 3. Intestinal alkaline phosphatase administration decreases intestinal NEC injury in a dose-dependent manner.

Conclusion: Early enteral supplemental IAP may reduce NEC-related injury and may be useful for preserving the intestinal epithelial barrier function.

MeSH terms

  • Administration, Oral
  • Alkaline Phosphatase / administration & dosage
  • Alkaline Phosphatase / therapeutic use*
  • Animals
  • Animals, Newborn
  • Claudin-1
  • Claudin-3
  • Claudins / biosynthesis
  • Claudins / genetics
  • Dextrans / pharmacokinetics
  • Dose-Response Relationship, Drug
  • Drug Evaluation, Preclinical
  • Enterocolitis, Necrotizing / drug therapy*
  • Enterocolitis, Necrotizing / etiology
  • Enterocolitis, Necrotizing / physiopathology
  • Fluorescein-5-isothiocyanate / analogs & derivatives
  • Fluorescein-5-isothiocyanate / pharmacokinetics
  • Gene Expression Regulation / drug effects
  • Ileum / drug effects*
  • Ileum / pathology
  • Intestinal Absorption / drug effects*
  • Intestinal Mucosa / drug effects*
  • Intestinal Mucosa / pathology
  • Lipopolysaccharides / toxicity
  • Membrane Proteins / biosynthesis
  • Membrane Proteins / genetics
  • Models, Animal
  • Permeability
  • Rats
  • Rats, Sprague-Dawley
  • Real-Time Polymerase Chain Reaction
  • Tight Junctions / drug effects

Substances

  • Claudin-1
  • Claudin-3
  • Claudins
  • Cldn1 protein, rat
  • Cldn3 protein, rat
  • Dextrans
  • Lipopolysaccharides
  • Membrane Proteins
  • fluorescein isothiocyanate dextran
  • Alkaline Phosphatase
  • Fluorescein-5-isothiocyanate