Helicobacter pylori enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in human gastric epithelial cells

Figure 1 Effects of TRAIL and H pylori on apoptosis in human gastric epithelial cell line AGS (^bP<0. 01 when compared with medium control, TRAIL or H pylori alone).

Figure 2 AGS cells incubated with heat killed, paraformalde-hyde-fixed (PA-fixed) or live H pylori (ATCC strain 43504) under the concentration of 4 × 10⁷ CFU/5 × 10⁴ cells for 12 h. Open bar: without TRAIL; filled bar: with TRAIL (^bP < 0.01).

Figure 3 Enhancement of TRAIL-mediated apoptosis by H pylori in primary human gastric epithelial cells.

Figure 4 Induction of TRAIL sensitivity specific for H pylori in human gastric epithelial cells (^bP < 0. 01 when compared with H pylori alone without adding TRAIL samples).

Figure 5 Enhancement of direct bacteria-cell contact depen-dent TRAIL sensitivity by H pylori (^bP < 0. 01).

Figure 6 Effects of vacA and cagA on induction of TRAIL sensitivity by H pylori. A: AGS cells (5 × 10⁴ cells) were incubated with a different concentration of H pylori (ATCC strain 51932) for 12 h. B: AGS cells were incubated with H pylori NTUH-C1 and its cagA, vacA gene knock out mutant strains (cagA KO, vacA KO) in the concentration of 4 × 10⁷ CFU/5 × 10⁴ cells for 12 h (^bP < 0.01 when compared with H pylori alone without adding TRAIL samples).

Figure 7 Expression of TRAIL on surface of T cells isolated from gastric mucosa.