Studies On The Interaction Of Helicobacter Pylori And AGS Cells At Different Time-points

Helicobacter pylori(H.pylori)colonizes the human stomach and is the causative agent of chronic gastris,peptic ulcer,and is closely related to gastric cancer.It has been recognized as a classâ… carcinogen by WHO at 1994.The type I strains harbor a 37KD cag pathogenicity island,while the typeâ…¡has no such regions.It is reported that the typeâ… strains are more inclined to induce gastric cancer in western countries.The samples of AGS cells co-cultured with H.pylori 26695 strain at different time-point were separated by 2-dimensional polyacrylamide gel electrophoresis (2-DE)technique and gene profile and computer-assisted image analysis were used to analyze the differential expression.CAM is the most significant perturbated pathway at every time-point,which MHCâ… ,MHCâ…¡,ICOS-Ligand(ICOSL),as well as the continued down-regulation ICAM3,may result in immune escape.The tight junction proteins called claudins involved in infection process,which CLDN15 down-regulation,and the early stage of infection CLDN2 and CLDN 23 up-regulation,and CLDN6 continued upward. Claudins can be used to determine the differentiation of gastric mucosa. Classification of gastric cancers using gastric and intestinal claudins is a good biomarker for assessing the risk of poor prognosis.The findings suggest that alterations in Claudin proteins are an early event in tumorigenesis and may provide targets for diagnosis and directed therapy for esophageal adenocarcinoma and its precursors.Second,different expression genes in the circadian rhythm and cell cycle pathway changes are also quite notable and suggested that the HP26695 infection can inhibit cell growth,making stranded in G1 cells/S phase.Phosphoinositide metabolism at the 4 h significant impact on their participation in the HP infection and inflammation regulate immune response.H.pylori 26695,cagA-positive strains,can active JNK and NF-kB pathways,which suggests that they may play a role in the pathogenic mechanism of cagA.There were 66 spots(34 proteins related)that were significantly differentially expressed at different time-point.Of those 34 protein spots,16 kinds of protein in all,8 proteins were increased obviously since the beginning of 2 h,in which 2 kinds of protein origined from the cells,and 6 kinds from HP;while other 4 kinds of cells origined protein expression down-regulated,with 4 new protein begined to express at 4h.Succinate dehydrogenase iron-sulfur subunit,HpaA,HSP 60 and peroxiredoxin 6 so on which were up-regulated in early stage.There were 4 kinds of protein expressioned at 4h,including cyclophilinA,nascent-polypeptide-associated complex alpha polypeptide,Urease and non-heme ferritin protein,which may be associated with the pathogenesis of H.pylori.The expression of proteome in AGS changes with time,such as in H.pylori.The interaction performed as the expression of protein associated with adhesion changed in early infection,and then followed by the trend favorable for the survival and proliferation of the H.pylori, demonstrating changes of immunologic escape and pathological erosion.The cell information transmission and the regulation are the foundation of the biological phenomena.The H.pylori-host interactions are time-depended.H.pylori 26695 and the AGS cell interaction is a dynamic change,and this research demonstrates sequential changes of them.And the key time-point is 4h.The sequential genome-wide expression profiles and the dynamic changes of protein provide very important clues for the epithelial cell migration,proliferation, circadian rhythm,apoptosis or carcinomatous change during H.pylori infection.