Fig. 2

Role of EVs induced by H. pylori infection in gastric and extragastric diseases. A Following H. pylori infection, EVs containing p-MET are released. They are then internalized by macrophages, which release pro-inflammatory cytokines that promote tumour growth and increase cell proliferation, migration and invasion. B MiR-155 exosomes from H. pylori-infected macrophages increased the production of the inflammatory cytokines IL-23, IL-6, IL-1βand TNF-α, in addition to the cell signalling proteins CD81, CD63, CD40 and MCH-I. Meanwhile, inflammatory signalling pathway proteins such as MyD88 and NF-kappaB have been downregulated in H. pylori-infected macrophages due to miR-155 overexpression. C H. pylori-derived exosomes upregulate the expression of soluble IL-6 receptor in GES-1 human gastric epithelial cells promoting the presentation of the pro-inflammatory cytokine IL-1α via its mediated IL-6 trans signal. D Serum exosomes derived from H. pylori-positive patients (Exo(Hp)) increased the expression of NLRP12 in intestinal epithelial cells, and NLRP12 reduced the expression of the chemokines MCP-1 and MIP-1α by inhibiting the Notch signalling pathway, ameliorating colitis symptoms. E CagA-containing exosomes derived from GES-1 human gastric epithelial cells regulate the expression of the tight junction protein claudin-2 at the transcriptional level via a CDX2-dependent mechanism, delaying the repair of the intestinal mucosa. F H. pylori induces gastric epithelial cell-derived exosomal miR-25 can enter the circulation and then regulate the NF-kappaB signaling pathway by targeting the transcription factor KLF2, leading to increased expression of ICAM-1, MCP-1, VCAM-1, and IL-6,, and accelerate the progression of atherosclerosis in vascular endothelial cells. G CagA in H. pylori-infected vascular endothelial cells-derived exosomes mediated reactive oxygen species(ROS) formation deregulates signals activating signal transducer and activator of JAK-STAT3 in endothelial cells, promoting atherogenesis. H CagA in exosomes derived from gastric epithelium infected with H. pylori induces the formation of macrophage foam cells and promotes atherosclerosis