AIM:To investigate the relations between tumor necrosisfactor-related apoptosis-inducing ligand (TRAIL) andHelicobacter pylori (H pylori) infection in apoptosis of gastricepithelial cells and to assess the expression of TRAIL onthe surface of infiltrating T-cells in Hpylori-infected gastricmucosa.METHODS:Human gastric epithelial cell lines and primarygastric epithelial cells were co-cultured with H pylori invitro,then recombinant TRAIL proteins were added to theculture.Apoptosis of gastric epithelial cells was determinedby a specific ELISA for cell death.Infiltrating lymphocyteswere isolated from Hpylori-infected gastric mucosa,andexpression of TRAIL in T cells was analyzed by flowcytometry.RESULTS:The apoptosis of gastric epithelial cell lines andprimary human gastric epithelial cells was mildly increasedby interaction with either TRAIL or Hpylorialone.Interestingly,the apoptotic indices were markedly elevated when gastricepithelial cells were incubated with both TRAIL and Hpylori(Control vsTRAIL and H pylori.0.51±0.06 vs 2.29±0.27,P=0.018).A soluble TRAIL receptor (DR4-Fc) couldspecifically block the TRAIL-mediated apoptosis.Furtherstudies demonstrated that infiltrating T-cells in gastricmucosa expressed TRAIL on their surfaces,and theinduction of TRAIL sensitivity by Hpyloriwas dependentupon direct cell contact of viable bacteria,but not CagAand VacA of H pylori.CONCLUSION:H pylori can sensitize human gastricepithelial cells and enhance susceptibility to TRAIL-mediatedapoptosis.Modulation of host cell sensitivity to apoptosisby bacterial interaction adds a new dimension to theimmunopathogenesis of H pylori infection. AIM: To investigate the relations between tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Helicobacter pylori (H pylori) infection in apoptosis of gastricepithelial cells and to assess the expression of TRAIL on the surface of infiltrating T-cells in Hpylori-infected gastric mucosa. METHODS: Human gastric epithelial cell lines and primary gastric epithelial cells were co-cultured with H pylori invitro, 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 Hpylori-infected gastric mucosa, andexpression 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 Hpylorialone. Tryteingly, the apoptotic indices were markedly elevated when gastricepithelial cells were incubated with both TRAIL and Hpylori (Con TRAIL-TRAIL receptor (DR4-Fc) couldspecifically block the TRAIL-mediated apoptosis. Furtherstudies demonstrated that infiltrating T-cells in gastric mucosa expressed TRAIL on their surfaces , and the induction of TRAIL sensitivity by Hpylori was dependentupon direct cell contact of viable bacteria, but not CagAand VacA of H pylori. CONCLUSION: H pylori can sensitize human gastricepithelial cells and enhance susceptibility to TRAIL-mediated apoptosis. Modulation of host cell sensitivity to apoptosisby bacterial interaction adds a new dimension to theimmunopathogenesis of H pylori infection.