title: Bifidobacterial supplementation reduces the incidence of necrotizing enterocolitis in a neonatal rat model.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Pediatrics, Northwestern University Medical School, Evanston Hospital, Evanston, Illinois, USA.
authors.forename: M S
authors.initials: MS
authors.lastname: Caplan
authors.forename: R
authors.initials: R
authors.lastname: Miller-Catchpole
authors.forename: S
authors.initials: S
authors.lastname: Kaup
authors.forename: T
authors.initials: T
authors.lastname: Russell
authors.forename: M
authors.initials: M
authors.lastname: Lickerman
authors.forename: M
authors.initials: M
authors.lastname: Amer
authors.forename: Y
authors.initials: Y
authors.lastname: Xiao
authors.forename: R
authors.initials: R
authors.lastname: Thomson
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D018988:Bacterial Translocation; D001644:Bifidobacterium / Q000502:physiology*; D002463:Cell Membrane Permeability; D004195:Disease Models, Animal; D004731:Endotoxins / Q000378:metabolism*; D020345:Enterocolitis, Necrotizing / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D007422:Intestines / Q000382:microbiology* / Q000473:pathology; D010741:Phospholipases A / Q000096:biosynthesis; D012333:RNA, Messenger; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D004731:Endotoxins; D012333:RNA, Messenger; D010741:Phospholipases A