Bifidobacterial supplementation reduces the incidence of necrotizing enterocolitis in a neonatal rat model

Gastroenterology. 1999 Sep;117(3):577-83. doi: 10.1016/s0016-5085(99)70450-6.


Background & aims: Neonatal necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature infants partly caused by intestinal bacterial proliferation. Because bifidobacteria are thought to reduce the risk for intestinal disturbances associated with pathogenic bacterial colonization, we hypothesized that exogenous bifidobacterial supplementation to newborn rats would result in intestinal colonization and a reduction in the incidence of neonatal NEC.

Methods: Newborn rat pups were given Bifidobacterium infantis (10(9) organisms per animal daily), Escherichia coli, or saline control and exposed to the NEC protocol consisting of formula feeding (Esbilac; 200 cal. kg(-1). day(-1)) and asphyxia (100% N(2) for 50 seconds followed by cold exposure for 10 minutes). Outcome measures included stool and intestinal microbiological evaluation, gross and histological evidence of NEC, plasma endotoxin concentration, intestinal phospholipase A(2) expression, and estimation of intestinal mucosal permeability.

Results: Bifidobacterial supplementation resulted in intestinal colonization by 24 hours and appearance in stool samples by 48 hours. Bifidobacteria-supplemented animals had a significant reduction in the incidence of NEC compared with controls and E. coli-treated animals (NEC, 7/24 B. infantis vs. 19/27 control vs. 16/23 E. coli; P < 0.01). Plasma endotoxin and intestinal phospholipase A(2) expression were lower in bifidobacteria-treated pups than in controls, supporting the role of bacterial translocation and activation of the inflammatory cascade in the pathophysiology of NEC.

Conclusions: Intestinal bifidobacterial colonization reduces the risk of NEC in newborn rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Bacterial Translocation
  • Bifidobacterium / physiology*
  • Cell Membrane Permeability
  • Disease Models, Animal
  • Endotoxins / metabolism*
  • Enterocolitis, Necrotizing / pathology
  • Enterocolitis, Necrotizing / physiopathology
  • Enterocolitis, Necrotizing / prevention & control*
  • Intestinal Mucosa / metabolism
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • Intestines / microbiology*
  • Intestines / pathology
  • Phospholipases A / biosynthesis
  • RNA, Messenger
  • Rats
  • Rats, Sprague-Dawley


  • Endotoxins
  • RNA, Messenger
  • Phospholipases A