Influence Of H. Pylori Infection On Duodenal Mucosal Epithelial Cell Bicarbonate Transport Protein

Objective：To investigate the expression of duodenal mucosal epithelial cell bicarbonatetransport protein(CFTR、SLC26A6、SLC26A3) in mice and cell,which were before andafter H. pylori infection,and to explore the cellular mechanisms whereby H. pyloriinfection influence duodenal mucosal epithelial cell bicarbonate secretion.Then elucidatepathogenesis of H. pylori correlation duodenal ulcer.Methods: Animal experiment: male C57BL/6J mice with the age of6weeks wererandomly divided into control group and model group, model group were fed by H.pyloristrains SS1（VacA+CagA+）,NCTC11637（VacA+CagA-）,NCTC11639（VacA-CagA+）.Gastric mucosae,which were taken at3days,1week,2week,4week,8week after H. pyloriinfection,were used to determine if infection was successfully by using RT-PCR andGiemsa staining.Then take the proximal duodenal mucosal, determine the mRNAexpression changes of duodenal mucosal bicarbonate transport protein（CFTR、SLC26A3、SLC26A6）by using RT-PCR. In vitro experiment: primary culture the duodenal mucosalepithelial cells of normal human，add to H.pylori strains after successfully culture andculture toghter for24hours. Then determine the mRNA expression changes of duodenalmucosal bicarbonate transport protein by using RT-PCR and Western-Blot.Results: Animal experiment: Giemsa staining shows a large number of H.pylori which arepurple-blue bodies with comma-shaped, short rod-shaped;16srRNA gene of H.pylori weredetermine by using RT-PCR.In model group,the mRNA expression of CFTR、SLC26A6、SLC26A3was significantly lower than the control group（P＜0.05）. In vitro experiment:The mRNA expression of CFTR、SLC26A6、SLC26A3decreased after culture toghter for24hours with H. pylori,which is compared with normal group（P＜0.05）.The proteinexpression of CFTR decreased after culture toghter for24hours with H. pylori,which is compared with normal group（P＜0.05）. Among them,the influence of SS1（VacA+CagA+） is large and lasting.Conclusion: H. pylori infection influenced the mRNA expression of duodenal mucosalepithelial cell bicarbonate transport protein, then influenced the bicarbonate secretion ofduodenal mucosal epithelial cell. This change relative to its pathogenic factor.