The Effect And Mechanism Of Lactobacillus On The Inflammatory Factor Of Gastritis Induced By Helicobacter Pylori

BackgroundHelicobacter pylori(H.pylori)is a spiral,flagellated,gram negative organism which colones in the gastric mucosa,affecting almost 50%of the world's population.H.pylori infection leads to chronic gastritis,peptic ulcer and gastric cancer.The World Health Organization has classified this bacterium as a class 1 carcinogen for gastric cancer.Nearly all patients,infected by H.pylori,had gastric mucosal inflammation,and the eradication of H.pylori can effectively reduce the inflammatory response of gastric mucosa,prevent the development of gastric mucosal atrophy and intestinal metaplasia,and decrease the risk of gastric cancer.To combine a proton pump inhibitor with two antibiotics and de-nol is the most effective measure to eradicate H.pylori.Due to the widesprea use of antiobiotics and the use of non-standard treatment,the drug resistence rate of H.pylori is increasing and the side effect of drug is a significant problem.Therefore,the search for new drugs and modified treatment has became an urgent problem.A large number of studies have indicated that probiotics can restrain H.pylori in vitro,make the eradication rate of H.pylori better,ameliorate the gastric mucosa inflammation,reduce drug side effects,and act as auxiliary treatment for H.pylori eradication.However,the molecular mechanism of probiotics treatment in H.pylori-induced gastritis is not clear.ObjectiveTwo strains of lactobacillus were used to interfere with animal models of H.pylori-induced gastritis and gastric cancer cell lines.The study investigated the molecular mechanism of lactobacillus treatment in H.pylori-induced gastritis,to provide new ideas for the prevention and treatment of H.pylori infection.Methods1?In vivo:Forty Blab/c mice were divided randomly into control group and test groups(H.pylori group,L.rhamnous DM9054+H.pylori group(L.rhamnous group),L.plantarum 86066+H.pylori group(L.plantarum group)).Balb/c mice of H.pylori infection was modeled by intragastric administration for two weeks.Then,L.rhamnous group and L.plantarum group were administered with(1�10~9CFU/ml,0.8ml)probiotics for 10 days;whereas,blank group and H.pylori group were given the same volume of normal saline for 10 days.The results of H.pylori coloning in Balb/c mice stomach were evaluated by rapid urease tests(RUT)and the number of H.pylori was calculated by colony-forming units per gram of stomach.The gastric inflammation was detected by hematoxylin and eosin staining(HE staining).2?In vitro,the AGS cells were treated with H.pylori and L.rhamnous or L.plantarum.The amount of IL-8 in cell culture medium was measured by ELISA,and IL-8 mRNA expression was analyzed by real-time PCR.The expression of total and phosphorylation forms of ERK1/2,JNK1/2,P38,JAK1,JAK2,STAT3,I?B-?and NF-?B p65 were measured by Western blot.Results1?In vivo,there was no H.pylori in the stomach of mice in blank group;however,H.pylori coloned in the stomach of mice in test groups and caused gastric inflammation.Compared with H.pylori group,there was no significant difference of coloning rate in the stomach of mice in L.rhamnous group or L.plantarum group(P>0.05).The inflammation in L.rhamnous group or L.plantarum group significantly decreased as compared with H.pylori group(P<0.05).2?In vitro:compared with the blank group,the levels of IL-8 in the cell supernatant and mRNA levels of IL-8 in AGS cells increased significantly in H.pylori group(P<0.05);and L.rhamnous DM9054 or L.plantarum 86066 decreased the protein and mRNA levels of IL-8(P<0.05).3?In vitro:compared with the blank group,the expressions of phosphorylation forms of ERK1/2,JNK1/2,P38,JAK1,JAK2,STAT3 and NF-?B p65 increased significantly in H.pylori group(P<0.05);and L.rhamnous DM9054 or L.plantarum86066 decreased the expressions of phosphorylation forms of ERK1/2,JNK1/2,P38?JAK1,JAK2,STAT3 and NF-?B p65(P<0.05).ConclusionL.rhamnous DM9054 or L.plantarum 86066 may inhibit H.pylori-induced gastritis by suppressing the expression of IL-8 through the inactivation of phosphorylation forms of proteins in the MAPK,JAK/STAT,and NF-?B pathways.