Galectin-9、Tim-3Expressions In Gastirc Mucosa Of Helicobacter Pyloir Infected Mongolian Gerbil

Background: The occurrence and development of a variety of uppergastrointestinal diseases is related to the Helicobacter pylori (H.pylori)infection. H.pylori has always been the focus of the study ofgastroenterology，since Barry J. Marshall and Robin Warren discovered andseparated from gastric biopsy samples successfully. After20years research,we has been confirmed that H. pylori is a major cause of chronic gastritis, animportant pathogenic factor for peptic ulcer, risk factors of gastric cancer, andan important cause of gastric mucosa-associated lymphoid tissue lymphoma. In1994, the world health organization/international cancer research organization(WHO/IARC) determined H. pylori as a kind of Carcinogenic factor. A seriesof pathophysiological changes will be caused after H. pylori colonization in thehuman body. Although after years of study, the pathophysiological changesand its mechanism is still not fully revealed. If H. pylori infectioned, the hostgastric mucosa will produce a chronic autoimmune pathological damageinstead of eradicate it, and then causing the infiltration of inflammatory cells,the development of chronic active gastritis, gastric atrophy, and ultimatelyinduced gastric cancer. Helper T cells which mediated cellular immuneresponses play a leading role in this process. Found in recent years, T cellimmuglobulin domain and mucin domain3(Tim-3) expressions indifferentiated Th1cells and Th17cells. And once evoked Th1reaction, Tim-3will be express in the final Th1cells, and through the IFN-γ induce Gal-9production, Gal-9in Th1cells trigger Tim-3terminate Th1immune response.And Gal-9can be induce Th1cells apoptosis.H.pylori infection caused byinfectious diseases characterized by chronic inflammation of Gal-9and Tim-3 expression levels has not been reported. The established Helicobacter pyloriinfection in Mongolian gerbils animal model of Mongolian gerbils in vivoGal-9, and Tim3reflect the changes.Research Objective: To establish animal model and to study Galectin-9,and Tim-3protein expressions in Mongolian gerbils infectioned by H.pylori.And Provide a theoretical basis for H.pylori infection immunotherapy.Methods:20clean-level Mongolian gerbils were randomly divided intocontrol and experimental groups (n=10), Pylori strains using ATCC43504(ofCagA+, Vac A+) the production of H. pylori infection in animal models ofMongolian gerbils, animals were sacrificed after12weeks of infection.Observe gastric tissue samples gross morphology，the detection of gastricjuice PH value, serological and pathological examination, and byimmunohistochemical detection of gastric mucosa in the Galectin-9and Tim3protein expression.Results: The experimental group of Mongolian gerbils gastric mucosavisible evidence of bleeding, chronic active gastritis and ulcers; lightmicroscope, a large number of chronic inflammatory cell invasion and theformation of lymphoid follicles gathered mainly lymphocytes, submucosa,blood vessels to dilate, congestive obviously, glandular atrophy and associatedwith epithelial cell degeneration and necrosis. Control group Mongolian gerbilsno H.pylori colonization and histological changes significantly; compared withthe control group, H.pylori infection Houmenggusha rat gastric mucosaGalectin-9protein expression levels were significantly lower Tim3proteinexpression increased.Conclusion:1，A stable H.pylori recovery and the establishment of the culture systemis successfully established the basis of H.pylori infection in Mongolian gerbilswith chronic gastritis animal models. 2， Expression of Galectin-9protein reduced in Mongolian gerbils gastricmucosa infected by H. pylori3, Tim-3protein expression was increased in H.pylori infectionMongolian gerbils gastric mucosa...