Table 2.

Key components of H. pylori OMVs and infected cell exosomes involved in pathogenesis and immune response.

Component	Type	Role in pathogenesis /immune response	Mechanistic Insights	Significance	References
VacA	OMV	Induces vacuole formation, modulates immune response, and promotes apoptosis in host cells	VacA enters host cells through endocytosis, resulting in the formation of large vacuoles. It inhibits T-cell activation and induces apoptosis in various immune cells, thereby contributing to immune evasion	Facilitates immune evasion and contributes to gastric pathology	(50, 56–59)
CagA	OMV/ Exosome	Alters host cell signaling pathways promote inflammation and are associated with gastric cancer	Disrupts host cell signaling and enhances inflammation	Enhances bacterial virulence and contributes to disease progression	(30, 51)
GGT	OMV	Induces immune tolerance	Contributes to cell-cycle arrest, apoptosis, and necrosis in gastric epithelial cells. Through the inhibition of T cell-mediated immunity and dendritic cell differentiation	Favoring persistent infection and gastric colonization	(34, 60–63)
LPS	OMV	Triggers strong inflammatory responses in host immune cells	Key roles in immune evasion and modulation	Plays a role in the inflammatory response to H. pylori infection	(5, 52, 64)
Outer membrane proteins (OMPs)	OMV	Involved in adhesion to host cells and immune evasion mechanisms	Facilitate host cell adhesion, immune evasion, and modulation of inflammatory responses	Critical for establishing and maintaining infection	(21, 65)
Exosomal microRNAs	Exosome	Modulate host immune responses and can induce immunosuppressive environments	Exosomal microRNAs derived from H. pylori can modulate the expression of genes involved in immune regulation and inflammation, enhancing bacterial persistence	Influence gene expression in host cells, contributing to immune modulation	(9, 37, 48, 66)
Phosphorylated mesenchymal-epithelial factor (p-MET)	Exosome	contributing to epithelial cell transition and inflammatory responses	Macrophages internalize this factor, resulting in elevated levels of IL-1β and IL-6 mRNA and increased IL-1α secretion, thereby fostering tumor growth	The presence of p-MET highlights the role of H. pylori in modulating host cell signaling pathways	(12)