Lactobacillus Rhamnosus GG Decreases Lipopolysaccharide -Induced Systemic Inflammation In A Gastrostomy-Fed Infant Rat Model

Objective To test whether LGG supplementation will decrease the pro-inflammatory response induced by E.coli Lipopolysaccharide in the infant rat small intestine, plasma, liver and lung.Methods Using a gastrostomy fed "pup-in-a-cup"rat model, the effects of supplemental LGG (108cfu/L·kg-1·day-1) were examined in the presence of LPS(0. 5mg · kg-1 · day-1). Two groups of 6-7d old pups were fed a rat milk substitute (RMS) via a gastrostomy tube providing 100% protein with and without additional LGG for another 7d. Mother fed rats at the same age was used as controls. Intestinal and plasma cytokine-induced neutrophil chemoattractant (CINC-1) and TNF α peptide were determined by ELISA. Inflammation response was determined with examination of microscopic pathology and myeloperoxidase (MPO) activity.Results LPS treatment blunted body growth, but LGG supplementation had no effect on weight increments. Sections of ileum from LPS-treated rat pups showed a striking metaplasia in the villous epithelium, these features were absent in the mother-reared control animals, and attenuated in the group treated with LPS plus LGG. LGG decreased LPS-induced inflammatory in intestinal tissue, CINC-1 (IL-8) production in plasma, liver, lung and distal small intestine(DSI), TNF α - production in plasma and lung and MPO activities in DSI and lung. Conclusion These results demonstrate that LGG provided by the enteral route is able to downregulate LPS induced proinflammatory mediators, and that this effect is not only present in the sphlanchnic organs, i.e., the intestine and liver, but extends to the plasma and a distal organ, the lung.