title: Lactobacillus rhamnosus GG decreases lipopolysaccharide-induced systemic inflammation in a gastrostomy-fed infant rat model.
abstract: OBJECTIVE
  A gastrostomy-fed rat infant "pup-in-a-cup" model was used to test the hypothesis that enterally administered Lactobacillus rhamnosus GG (LGG) decreases the proinflammatory response induced by Escherichia coli lipopolysaccharide (LPS) in the developing infant rat small intestine, plasma, lung and liver.
  
  
  METHODS
  Two groups of 6- to 7-day-old pups were fed a rat milk substitute with LPS added via the gastrostomy tube for 6 days. One of the rat milk substitute-fed groups received supplemental LGG; another group received LPS without LGG. Age-matched mother-fed rat pups were used as controls.
  
  
  RESULTS
  LPS treatment blunted body growth, but LGG supplementation had no effect on weight increments. LGG decreased LPS-induced inflammation in intestinal tissue; CINC-1 (rodent IL-8 equivalent) production in plasma, liver, lung and distal small intestine; and tumor necrosis factor alpha (TNF-alpha) production in plasma and lung. Cytokine multiplex assay showed lung interleukin (IL)-1beta, IL-6, IL-10, IL-18, growth-related oncogene (GRO)/KC (rat CINC-1) and TNF-alpha were significantly higher in gastrostomy-fed, LPS-treated pups than in mother-reared pups, and LGG significantly blunted the LPS-induced elevation of IL-1beta, IL-10, IL-18, GRO/KC and TNF-alpha; liver GRO/KC was significantly higher in gastrostomy-fed, LPS-treated pups than in mother-reared pups, and LGG significantly blunted the LPS-induced elevation of GRO/KC.
  
  
  CONCLUSIONS
  LGG provided by the enteral route is able to downregulate LPS-induced proinflammatory mediators. This effect is not only present in the splanchnic organs, that is, the intestine and the liver, but extends to the plasma and a distal organ, the lung.
authors.affiliation: Department of Neonatology, Fujian Provincial Maternity and Children Health Hospital, Fuzhou, Fujian Province, China, 350001.
authors.forename: Liyan
authors.initials: L
authors.lastname: Zhang
authors.forename: Nan
authors.initials: N
authors.lastname: Li
authors.forename: Clotilde
authors.initials: C
authors.lastname: des Robert
authors.forename: Maozhong
authors.initials: M
authors.lastname: Fang
authors.forename: Kellym
authors.initials: K
authors.lastname: Liboni
authors.forename: Robert
authors.initials: R
authors.lastname: McMahon
authors.forename: Ricardo A
authors.initials: RA
authors.lastname: Caicedo
authors.forename: Josef
authors.initials: J
authors.lastname: Neu
mesh_terms: D000818:Animals; D016207:Cytokines / Q000032:analysis / Q000276:immunology*; D015536:Down-Regulation; D004750:Enteral Nutrition; D004926:Escherichia coli / Q000276:immunology*; D005774:Gastrostomy; D007249:Inflammation / Q000276:immunology* / Q000382:microbiology; D007421:Intestine, Small / Q000276:immunology; D052201:Lacticaseibacillus rhamnosus / Q000276:immunology; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000276:immunology*; D008099:Liver / Q000276:immunology; D008168:Lung / Q000276:immunology; D023421:Models, Animal; D010949:Plasma / Q000276:immunology; D019936:Probiotics / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides