Fig. 1

Various mechanisms of H. pylori outer membrane vesicles (OMVs)-mediated immune responses: (1) H. pylori OMVs induce ICAM-1 (intracellular adhesion molecule)-1 and CD11b (integrin) expression, causing degranulation and ECP (eosinophil cationic protein) release; (2) neutrophil activation via G-protein pathway involving GPCR (G-protein-coupled receptor) and kinases, resulting in oxidative burst and reactive oxygen species (ROS) production due to NADPH oxidase activation; (3) nuclear factor (NF)-κB activation and cytokine release by monocytes involve Toll-like receptor (TLR)4 and CD14 binding with H. pylori ligands delivered by OMV’S; (4) the increase in T-cell activation and cytokine secretion including TNF (tumor necrosis factor)-α and interferon (IFN)-γ during H. pylori infection stimulate the release of proinflammatory cytokines such as interleukin (IL)-8 from gastric epithelium through NFκB activation pathway