细菌源性细胞外囊泡（EV）已成为宿主和病原体之间相互作用的关键介质，在传染病和癌症中发挥着重要作用。在这些病原体中，幽门螺杆菌（H. pylori）是一种特别重要的细菌，与各种胃肠道疾病、胃癌和全身性疾病有关。幽门螺杆菌通过刺激宿主细胞分泌 EV 并产生内外膜囊泡 (OMV) 来实现这些效果。来自幽门螺杆菌感染的宿主细胞的EV可调节炎症信号通路，从而影响细胞增殖、凋亡、细胞因子释放、免疫细胞修饰和内皮功能障碍，并破坏细胞连接结构并诱导细胞骨架重组。此外，从幽门螺杆菌中分离出的 OMV 在形成随后的免疫病理反应中发挥着关键作用。这些囊泡在宿主环境中引发炎症和免疫抑制反应，促进病原体逃避宿主防御和入侵宿主细胞。尽管人们的认识不断加深，但涉及幽门螺杆菌衍生的电动汽车的研究仍处于不同领域的早期阶段。在这篇综合综述中，我们介绍了阐明 EV 成分（例如非编码 RNA (ncRNA) 和蛋白质）对胃部和胃外疾病发病机制的贡献的最新进展。此外，我们强调了它们作为生物标志物、治疗靶点和靶向递送载体的潜在效用。© 2023。作者。

Bacterial-derived extracellular vesicles (EVs) have emerged as crucial mediators in the cross-talk between hosts and pathogens, playing a significant role in infectious diseases and cancers. Among these pathogens, Helicobacter pylori (H. pylori) is a particularly important bacterium implicated in various gastrointestinal disorders, gastric cancers, and systemic illnesses. H. pylori achieves these effects by stimulating host cells to secrete EVs and generating internal outer membrane vesicles (OMVs). The EVs derived from H. pylori-infected host cells modulate inflammatory signaling pathways, thereby affecting cell proliferation, apoptosis, cytokine release, immune cell modification, and endothelial dysfunction, as well as disrupting cellular junctional structures and inducing cytoskeletal reorganization. In addition, OMVs isolated from H. pylori play a pivotal role in shaping subsequent immunopathological responses. These vesicles incite both inflammatory and immunosuppressive reactions within the host environment, facilitating pathogen evasion of host defenses and invasion of host cells. Despite this growing understanding, research involving H. pylori-derived EVs remains in its early stages across different domains. In this comprehensive review, we present recent advancements elucidating the contributions of EV components, such as non-coding RNAs (ncRNAs) and proteins, to the pathogenesis of gastric and extragastric diseases. Furthermore, we highlight their potential utility as biomarkers, therapeutic targets, and vehicles for targeted delivery.© 2023. The Author(s).