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Expression And Significance Of Toll-like Receptor 2,4,5 In The Gastritis And Gastric Ulcer With Helicobacter Pylori Infected

Posted on:2017-12-25Degree:MasterType:Thesis
Country:ChinaCandidate:K K QinFull Text:PDF
GTID:2334330485998579Subject:Internal Medicine
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Objective:In order to clarify the role of toll-like receptors 2,4,5 and the signaling pathways in the immune response in the process of gastritis and gastric ulcer disease caused by Helicobacter pylori.This experiment treated the patients with gastritis or gastric ulcer and the normal group who were classificaed on the basis of whether H.pylori existed or not.We detected he expression of Toll like receptors 2,4,5 and the key factors in signal transduction myeloid differentiation factor and nuclear factor kappa B in the above groups.Further more,we observed the effect of the eradication of Helicobacter pylori on the expression of above factors in the different gastric epithelia.Methods:Biopsy specimens were obtained from the gastric mucosal of 88 cases of chronic gastritis,82 cases of gastric ulcer and 80 cases of normal control group by the electronic gastroscopy and biopsy forceps.Rapid urea test and carbon 13 breath test were performed to observe the infection rates of Helicobacter pylori.And then we selected the Helicobacter pylori positive patients with gastritis and gastric ulcer,who were treated with the triple therapy for eradication of Helicobacter pylori in a course of 2 weeks.The treatment plan was rabeprazole 10 mg,2 times / day + amoxicillin 1000 mg,2 times / day + clarithromycin 500 mg,2 times / day.After 4 weeks of drug withdrawal the gastroscopy was performed again,this time we detected the Helicobacter pylori and collected the gastric mucosal tissue like last time.The expressions of TLR2,4,5,NF-?B and MyD88 mRNAs were detected by real-time quantitative polymerase chain reaction.all the datas were analysised by the SPSS17.0 software,Measurement datas were treated with the t/t?-test and the One-Way ANOVA testand enumeration datas were treated with the chi-square test,it was significant statistical difference if P<0.05.Results:H.pylori infection rates in the gastric ulcer group,gastritis group and control group were 75.6%,64.5%,52.5% respectively,the differences of them were statistiacl significance(?2 = 9.44,P =0.009 <0.05).The normal gastric mucosa was damaged in different degrees in the patients with gastritis and gastric ulcer by the endoscopic results and the histopathological sections of the gastric mucosa tissue demonstrates infiltration with neutrophils and monocytic.The expression levels of TLR2?4,NF-?B and MyD88 mRNA were significantly higher in the H.pylori positive group than the H.Pylori negative groups,(P<0.05).Smilarly,no matter in the H.pylori positive group or in the H.pylori negative groups,gastric ulcer group showed significantly stronger expressions of TLR2,4,NF-?B and MyD88 mRNAs compared with the gastritis group and normal group(P <0.05),gastritis group is also higher than normal group with statistical significance(P < 0.05).Expression of TLR5 was no significant difference between gastritis group and control group and had no related to H.pylori infection.However,expression of the ulcer group increasesed significantly than others.After the eradication of H.pylori,the endoscopic and pathological manifestations of patients were significantly improved,and expressions of TLR2,?4,MYD88 and nuclear factor kappa B were also decreased significantly than before,but expression of TLR5 shew no obvious variation between gastritis group and the control in this period.Conclusion:H.pylori associated gastritis and gastric ulcer concerned with the immune response mediated by TLR2,4.H.Pylori may activate TLR2 and 4 through its own pathogenetic agent and the latter could activate MYD88.MYD88 can raise different downstream signaling factors and initiate the nucleus gene expression by activating NF-?B and then the excessive delivery of cytokines and inflammatory mediators induce inflammatory reaction loss of control and immune function disorder which may induce the begin and development of the gastric mucosal diseases.what?s more,the inflammation reaction can be activated and boosted by the throught some mechanisms to up-regulate the expression TLR2?4,but TLR5 plays a negligible role in early start of the process it revealed that flagellum may be not the major virulence factor in this time.Eradication of H.pylori can reduce the expression of TLR2,4 and its signal factors,thus TLR2?4 and key factors in signal transduction provide a reliable therapeutic target,the study aimed at them may provide the beneficial basis for the future treatment of the gastric mucosal diseases caused by Helicobacter pylori infection.
Keywords/Search Tags:Gastritis, Gastric ulcer, Toll-like receptors, Myeloid differentiation factor 88, Helicobacter pylori
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