title: Bifidobacterium longum subsp. infantis in experimental necrotizing enterocolitis: alterations in inflammation, innate immune response, and the microbiota.
abstract: BACKGROUND
  Probiotics decrease the risk of necrotizing enterocolitis (NEC). We sought to determine the impact of Bifidobacterium longum subsp. infantis (B. infantis) in the established rat model of NEC.
  
  
  METHODS
  Rat pups delivered 1 d prior to term gestation were assigned to one of three groups: dam fed (DF), formula fed (FF), or fed with formula supplemented with 5 × 10(6) CFU B. infantis per day (FF+Binf). Experimental pups were exposed to hypoxia and cold stress. Ileal tissue was examined for pathology and expression of inflammatory mediators, antimicrobial peptides, and goblet-cell products. Ceca were assessed for bacterial composition by analysis of the 16S rRNA sequence.
  
  
  RESULTS
  Administration of B. infantis significantly reduced the incidence of NEC, decreased expression of Il6, Cxcl1, Tnfa, Il23, and iNOS, and decreased expression of the antimicrobial peptides Reg3b and Reg3g. There was significant microbial heterogeneity both within groups and between experiments. The cecal microbiota was not significantly different between the FF and FF+Binf groups. Bifidobacteria were not detected in the cecum in significant numbers.
  
  
  CONCLUSIONS
  In the rat model, the inflammation associated with NEC was attenuated by administration of probiotic B. infantis. Dysbiosis was highly variable, precluding determination of the precise role of the microbiota in experimental NEC.
authors.affiliation: Department of Pediatrics, University of California, Davis, Sacramento, California.
authors.forename: Mark A
authors.initials: MA
authors.lastname: Underwood
authors.affiliation: Department of Pediatrics and the Steele Children's Research Center, The University of Arizona, Tucson, Arizona.
authors.forename: Jennifer
authors.initials: J
authors.lastname: Arriola
authors.affiliation: Department of Pediatrics and the Steele Children's Research Center, The University of Arizona, Tucson, Arizona.
authors.forename: Colin W
authors.initials: CW
authors.lastname: Gerber
authors.affiliation: Department of Pediatrics and the Steele Children's Research Center, The University of Arizona, Tucson, Arizona.
authors.forename: Ashwini
authors.initials: A
authors.lastname: Kaveti
authors.affiliation: Department of Viticulture and Enology, University of California, Davis, Davis, California.
authors.forename: Karen M
authors.initials: KM
authors.lastname: Kalanetra
authors.affiliation: Department of Medical Microbiology and Immunology, University of California, Davis, Davis, California.
authors.forename: Anchasa
authors.initials: A
authors.lastname: Kananurak
authors.affiliation: Department of Medical Microbiology and Immunology, University of California, Davis, Davis, California.
authors.forename: Charles L
authors.initials: CL
authors.lastname: Bevins
authors.affiliation: Department of Viticulture and Enology, University of California, Davis, Davis, California.
authors.forename: David A
authors.initials: DA
authors.lastname: Mills
authors.affiliation: Department of Pediatrics and the Steele Children's Research Center, The University of Arizona, Tucson, Arizona.
authors.forename: Bohuslav
authors.initials: B
authors.lastname: Dvorak
mesh_terms: D000818:Animals; D001644:Bifidobacterium / Q000235:genetics / Q000502:physiology*; D002432:Cecum / Q000382:microbiology; D020345:Enterocolitis, Necrotizing / Q000628:therapy*; D007113:Immunity, Innate / Q000502:physiology*; D007249:Inflammation / Q000628:therapy*; D064307:Microbiota; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D051381:Rats
chemical_list: D012336:RNA, Ribosomal, 16S