Skip to main content
. 2024 Jul 31;14:1416819. doi: 10.3389/fcimb.2024.1416819

Figure 1.

Figure 1

Apoptosis and Necroptosis in H. pylori infection. In the intrinsic pathway of apoptosis, only BH3 proteins are upregulated after H. pylori infection. They interact with the BCL-2 proteins, which are essential for survival, and thus override the inhibition of BAX and BAK. As a result, BAX and BAK oligomerize, leading to MOMP. After its release into the cytoplasm, cytochrome c binds to Apaf-1, which activates the initiator caspases and induces apoptosis. VacA, which causes the translocation of BAX and increases cytochrome c, can also enhance apoptosis. BID is one of the pure BH3 proteins. It can be cleaved by activated caspase-8 and releases BAX and BAK to activate intrinsic apoptosis via the MOMP pathway. In the extrinsic pathway, H. pylori promotes the formation of pAbIT735 via the type IV secretion system (T4SS), thereby attenuating caspase-8-dependent cell apoptosis. In necroptosis, infection with H. pylori leads to an increase in the key factor RIPK3, which promotes the occurrence of inflammatory reactions. VacA also triggers necroptosis and releases considerable amounts of inflammatory mediators.