| Yi-Ying Wu |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=3.300 ------>paper_class3=2 ------>paper_class2=1 ------>vol=10 ------>confirm_bywho=None ------>insert_bywho=hftsai ------>Jurnal_Rank=35.0 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=2339 ------>medlineContent= ------>unit=000 ------>insert_date=20081204 ------>iam=2 ------>update_date=None ------>author=??? ------>change_event=1 ------>ISSN= ------>authors_c= ------>score=472 ------>journal_name=World J Gastroenterol. ------>paper_name=Helicobacter pylori enhances tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in human gastric epithelial cells ------>confirm_date=None ------>tch_id=097069 ------>pmid=15285015 ------>page1=2334 ------>fullAbstract=AIM: To investigate the relations between tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Helicobacter pylori (H pylori) infection in apoptosis of gastric epithelial cells and to assess the expression of TRAIL on the surface of infiltrating T-cells in H pylori-infected gastric mucosa. METHODS: Human gastric epithelial cell lines and primary gastric epithelial cells were co-cultured with H pylori in vitro, then recombinant TRAIL proteins were added to the culture. Apoptosis of gastric epithelial cells was determined by a specific ELISA for cell death. Infiltrating lymphocytes were isolated from H pylori-infected gastric mucosa, and expression of TRAIL in T cells was analyzed by flow cytometry. RESULTS: The apoptosis of gastric epithelial cell lines and primary human gastric epithelial cells was mildly increased by interaction with either TRAIL or H pylori alone. Interestingly, the apoptotic indices were markedly elevated when gastric epithelial cells were incubated with both TRAIL and H pylori (Control vs TRAIL and H pylori: 0.51+/-0.06 vs 2.29+/-0.27, P = 0.018). A soluble TRAIL receptor (DR4-Fc) could specifically block the TRAIL-mediated apoptosis. Further studies demonstrated that infiltrating T-cells in gastric mucosa expressed TRAIL on their surfaces, and the induction of TRAIL sensitivity by H pylori was dependent upon direct cell contact of viable bacteria, but not CagA and VacA of H pylori. CONCLUSION: H pylori can sensitize human gastric epithelial cells and enhance susceptibility to TRAIL-mediated apoptosis. Modulation of host cell sensitivity to apoptosis by bacterial interaction adds a new dimension to the immunopathogenesis of H pylori infection. ------>tmu_sno=None ------>sno=20458 ------>authors2=Hwei-Fang Tsai ------>authors3=We-Cheng Lin ------>authors4=Ai-Hsiang Chou ------>authors5=Hui-Ting Chen ------>authors6=Jyh-Chin Yang,Ping-I Hsu, Ping-Ning Hsu. ------>authors6_c= ------>authors=Yi-Ying Wu ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Helicobacter pylori enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in human gastric epithelial cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2004 ------>submit_flag=None ------>publish_month=1 |