Fig. 7.

Proposed model for the mechanism of apoptosis induction by H. pylori in AGS gastric epithelial cells. Activation of death receptors by H. pylori results in the initial cleavage of procaspase-8 to generate caspase-8. Caspase-8 represents a branch point, activating caspase-6 in one direction and cleaving Bid in another direction. Increased levels proapoptotic Bcl-2 family members (e.g., Bak) facilitate a change in mitochondrial membrane potential (Δψm), leading to the release of AIF. As a consequence, nuclear lamins are cleaved, leading to nuclear condensation and apoptosis.