Figure 1.

Generally, H. pylori adheres to gastric mucosa epithelial cells via the outer membrane protein and injects CagA into host cells via a type IV secretory system, resulting in changes in cytokine signaling and cell cycle control. When the external environment changes and becomes unfavorable, H. pylori invades the epithelial cells and multiplies in double-layer membrane vesicles to seek refuge. After internalization, autophagosomes form to degrade some of the ingested bacteria. Once the external environment becomes favorable, undegraded H. pylori is released from host cells into the external environment for recolonization.