Bifidobacterium bifidum in a rat model of necrotizing enterocolitis: antimicrobial peptide and protein responses

Mark A Underwood1, Anchasa Kananurak, Christine F Coursodon

  • 1Department of Pediatrics, University of California-Davis, Sacramento, California, USA. mark.underwood@ucdmc.ucdavis.edu

Pediatric Research
|February 11, 2012
PubMed

Insights

Probiotics like Bifidobacterium bifidum reduce the risk of necrotizing enterocolitis (NEC) in premature infants by modulating antimicrobial peptide expression. This study shows probiotics help prevent NEC by regulating these gut peptides.

Area of Science:

  • Gastroenterology
  • Neonatology
  • Microbiology

Background:

  • Necrotizing enterocolitis (NEC) is a severe intestinal disease affecting premature infants.
  • Probiotics are known to reduce NEC risk, but their effect on antimicrobial peptides in NEC is not well understood.

Purpose of the Study:

  • To examine antimicrobial peptide expression in experimental NEC.
  • To determine how probiotics influence antimicrobial peptide levels in NEC.

Main Methods:

  • Premature rats were divided into dam-fed, formula-fed, and formula-fed with Bifidobacterium bifidum groups.
  • All groups were subjected to asphyxia and cold stress to induce NEC-like conditions.
  • Antimicrobial peptide gene expression was analyzed in the different experimental groups.

Main Results:

  • Antimicrobial peptide expression was significantly elevated in formula-fed rats with NEC compared to controls.
  • Probiotic supplementation with Bifidobacterium bifidum attenuated NEC and reduced the elevated antimicrobial peptide levels.
  • Antimicrobial peptide expression in rat pups mirrored patterns seen in human development, increasing with age.

Conclusions:

  • Antimicrobial peptide induction is a response to experimental NEC, similar to human disease.
  • Probiotic B. bifidum mitigates experimental NEC and normalizes antimicrobial peptide expression.
  • While an adaptive response, antimicrobial peptides alone may not be sufficient to prevent NEC in the vulnerable premature gut.
Abstract