AIM:To determine the protective effect of triple viable probiotics on gastritis induced by Helicobacter pylori(H.pylori) and elucidate the possible mechanisms of protection.METHODS:Colonization of BIFICO strains in the mouse stomach was determined by counting colony-forming units per gram of stomach tissue.After treatment with or without BIFICO,inflammation and H.pylori colonization in the mouse stomach were analyzed by hematoxylin and eosin and Giemsa staining,respectively.Cytokine levels were determined by enzyme-linked immunosorbent assay and Milliplex.The activation of nuclear factor(NF)-κB and MAPK signaling in human gastric epithelial cells was evaluated by Western blot analysis.Quantitative reverse transcription-polymerase chain reaction was used to quantify TLR2,TLR4 and MyD 88 mR NA expression in the mouse stomach.RESULTS:We demonstrated that BIFICO,which contains a mixture of Enterococcus faecalis,Bifidobacterium longum and Lactobacillus acidophilus,was tolerant to the mouse stomach environment and was able to survive both the 8-h and 3-d courses of administration.Although BIFICO treatment had no effect on the colonization of H.pylori in the mouse stomach,it ameliorated H.pylori-induced gastritis by significantly inhibiting the expression of cytokines and chemokines such as TNF-α,IL-1β,IL-10,IL-6,G-CSF and MIP-2(P < 0.05).These results led us to hypothesize that BIFICO treatment would diminish the H.pylori-induced inflammatory response in gastric mucosal epithelial cells in vitro via the NF-κB and MAPK signaling pathways.Indeed,we observed a decrease in the expression of the NF-κB subunit p65 and in the phosphorylation of IκB-α,ERK and p38.Moreover,there was a significant decrease in the production of IL-8,TNF-α,G-CSF and GM-CSF(P <0.05),and the increased expression of TLR2,TLR4 and My D88 induced by H.pylori in the stomach was also significantly reduced following BIFICO treatment(P <0.05).CONCLUSION:Our results suggest that the probiotic cocktail BIFICO can ameliorate H.pylori-induced gastritis by inhibiting the inflammatory response in gastric epithelial cells. AIM: To determine the protective effect of triple viable probiotics on gastritis induced by Helicobacter pylori (H. pylori) and elucidate the possible mechanisms of protection. METHODS: Colonization of BIFICO strains in the mouse stomach was determined by counting colony-forming units per gram of stomach tissue. After treatment with or without BIFICO, inflammation and H. pylori colonization in the mouse stomach were analyzed by hematoxylin and eosin and Giemsa staining, respectively. Cytokine levels were determined by enzyme-linked immunosorbent assay and Milliplex. The activation of nuclear factor (NF) -κB and MAPK signaling in human gastric epithelial cells was evaluated by Western blot analysis. Quantitative reverse transcription-polymerase chain reaction was used to quantify TLR2, TLR4 and MyD 88 mR NA expression in the mouse stomach .RESULTS: We say that BIFICO, which contains a mixture of Enterococcus faecalis, Bifidobacterium longum and Lactobacillus acidophilus, was tolerant to the mouse stomach environment and was able to survive both the 8-h and 3-d courses of administration. Although BIFICO treatment had no effect on the colonization of H. pylori in the mouse stomach, it ameliorated H. pylori-induced gastritis by significantly inhibiting the expression of cytokines and chemokines such as TNF-α, IL-1β, IL-10, IL-6, G-CSF and MIP-2 (P <0.05). pylori-induced inflammatory response in gastric mucosal epithelial cells in vitro via the NF-κB and MAPK signaling pathways. Indeed, we observed a decrease in the expression of the NF-κB subunit p65 and in the phosphorylation of IκB-α, ERK and p38 . Moreover, there was a significant decrease in the production of IL-8, TNF-α, G-CSF and GM-CSF (P <0.05), and the increased expression of TLR2, TLR4 and My D88 induced by H. pylori in the stomach was also significantly reduced following the BIFICO treatment (P <0.05) .CONCLUSION: Our results suggest that the probiotic cocktail BIFICO can ameliorate H. pylori-induced gastritis by inhibiting the inflammatory response in gastric epithelial cells.