[HTML][HTML] Bifidobacterium longum subsp. infantis in experimental necrotizing enterocolitis: alterations in inflammation, innate immune response, and the microbiota
MA Underwood, J Arriola, CW Gerber, A Kaveti… - Pediatric …, 2014 - nature.com
MA Underwood, J Arriola, CW Gerber, A Kaveti, KM Kalanetra, A Kananurak, CL Bevins…
Pediatric research, 2014•nature.comBackground: 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 …
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 …
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.
Conclusion:
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.
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