Intestinal barrier dysfunction in human necrotizing enterocolitis

J Pediatr Surg. 2016 Dec;51(12):1907-1913. doi: 10.1016/j.jpedsurg.2016.09.011. Epub 2016 Sep 15.

Abstract

Background: Intestinal barrier dysfunction has been implicated in necrotizing enterocolitis (NEC), but has not been directly measured in human NEC.

Methods: Small intestines removed during surgery were immediately mounted in an Ussing chamber. mRNA expression of tight junction (TJ) proteins was measured with RT-PCR.

Results: Fifteen infants were included, 5 with NEC and 10 with other diagnoses. Average transepithelial resistance (TER) was 11.61±1.65Ω/cm2 in NEC specimens, 23.36±1.48Ω/cm2 at resection margin, and 46.48±5.65Ω/cm2 in controls. Average flux of permeability marker mannitol was 0.23±0.06μMol/cm2 per h in NEC, 0.04±0.01 μMol/cm2 per h at resection margin, and 0.017±0.004 μMol/cm2 per h in control tissue (p<0.05). RT-PCR analysis showed marked decrease in mRNA expression of a TJ protein occludin in NEC affected tissue (p<0.03 vs. control). Additionally, mRNA expression of myosin light chain kinase (MLCK), an important regulator of TJ permeability, was increased in NEC specimens.

Conclusion: These studies show for the first time that NEC intestinal tissue have increased intestinal permeability, even at grossly healthy-appearing resection areas. The increase in intestinal permeability in NEC appeared to be related in part to a decrease in occludin and an increase in MLCK expression.

Level of evidence: Level 2.

Keywords: Intestinal barrier function; Necrotizing enterocolitis; Occludin; Tight junction.

MeSH terms

  • Enterocolitis, Necrotizing / metabolism
  • Enterocolitis, Necrotizing / physiopathology*
  • Female
  • Humans
  • Infant
  • Infant, Newborn
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / physiopathology*
  • Intestine, Small / metabolism
  • Intestine, Small / physiopathology*
  • Male
  • Myosin-Light-Chain Kinase / biosynthesis
  • Occludin / biosynthesis
  • Permeability
  • RNA, Messenger / biosynthesis
  • Tight Junctions / metabolism*

Substances

  • Occludin
  • RNA, Messenger
  • Myosin-Light-Chain Kinase