OBJECTIVES: Helicobacter pylori (HP) infection has been reported to accelerate the apoptosis of gastric epithelial cells. This bacteria has also been known to enhance the expression levels of molecules such as Fas antigen and a receptor for tumor necrosis factor-alpha-receptor type 1 (TNF-R1). However, whether Fas and/or TNF-R1 is actually involved in HP-mediated apoptosis has yet to be evaluated. The purpose of this study was therefore to examine the roles of Fas and TNF-R1 in HP-mediated apoptosis. METHODS: Biopsy samples were collected from 10 HP-negative healthy volunteers and from 39 HP-positive ulcer patients. Gastric epithelial cells were obtained from the samples. The cells were then stained with anti-Fas, anti-TNF-R1 and Annexin V, which detected apoptotic cells. The findings were analyzed by three-color flow cytometry. RESULTS: The percentages of apoptotic cells were significantly higher in HP-positive patients than in the controls. In HP-negative controls, almost all of the apoptotic cells lacked both Fas and TNF-R1. On the other hand, in HP-positive patients, HP upregulated the expression levels of Fas and TNF-R1 and, consequently, enhanced the apoptosis mediated by receptors such as Fas and TNF-R1. However, even in HP-positive patients, apoptosis was also observed in the cells that lacked both Fas and TNF-R1. CONCLUSIONS: Fas and TNF-R1 expressed on gastric epithelial cells from HP-infected patients were responsible for the accelerated apoptosis of the cells.
OBJECTIVES:Helicobacter pylori (HP) infection has been reported to accelerate the apoptosis of gastric epithelial cells. This bacteria has also been known to enhance the expression levels of molecules such as Fas antigen and a receptor for tumor necrosis factor-alpha-receptor type 1 (TNF-R1). However, whether Fas and/or TNF-R1 is actually involved in HP-mediated apoptosis has yet to be evaluated. The purpose of this study was therefore to examine the roles of Fas and TNF-R1 in HP-mediated apoptosis. METHODS: Biopsy samples were collected from 10 HP-negative healthy volunteers and from 39 HP-positive ulcerpatients. Gastric epithelial cells were obtained from the samples. The cells were then stained with anti-Fas, anti-TNF-R1 and Annexin V, which detected apoptotic cells. The findings were analyzed by three-color flow cytometry. RESULTS: The percentages of apoptotic cells were significantly higher in HP-positive patients than in the controls. In HP-negative controls, almost all of the apoptotic cells lacked both Fas and TNF-R1. On the other hand, in HP-positive patients, HP upregulated the expression levels of Fas and TNF-R1 and, consequently, enhanced the apoptosis mediated by receptors such as Fas and TNF-R1. However, even in HP-positive patients, apoptosis was also observed in the cells that lacked both Fas and TNF-R1. CONCLUSIONS:Fas and TNF-R1 expressed on gastric epithelial cells from HP-infectedpatients were responsible for the accelerated apoptosis of the cells.