The interaction between Helicobacter pylori and autophagy: A putative mechanism involved in gastric carcinogenesis

Helicobacter pylori is a Gram-negative bacterium that colonizes the gastric tissue of more than half of the world's population and is the major risk factor for the development of gastric cancer.  H. pylori is the most common bacterial pathogen in humans, and there is a significant association  between H. pylori infection and gastric cancer. Autophagy is a protective process used by  eukaryotic cells to maintain cell homeostasis and defend against the attack of pathogenic    microbes. H. pylori can induce autophagy in epithelial cells of the stomach and professional  phagocytes such as macrophages and dendritic cells. Tumor inhibitory proteins including   phosphatases, PTEN, P53, and retinoblastoma protein have a positive effect on autophagy   regulation. In comparison, oncogenic products such as BCL-2 and AKT/TOR pathways play an inhibitory role on autophagy. However, the relationship between regulation of autophagy and   tumorigenesis is still unclear. During H. pylori infection and after the induction of autophagy, the bacterium can escape this process by downregulation of autophagy-related proteins, and/or use the autophagosome as a suitable niche for intracellular survival. In addition, autophagy can cause cell survival or cell death through the gastric cancer process. In conclusion, the role of H. pylori  infection in induction or inhibition of autophagy process, and its impact on gastric carcinogenic related pathways are a matter of controversy, which need further studies to understand the   interactions between the microbe and autophagy.