H.pylori is an important factor in GC and triggers chronic inflammation. The role of
H.pylori -derived EVs have been identified (Fig.
4). CagA (Cytotoxin-associated gene A) is a major virulence factor in
H.pylori. In gastric juices from GC patients,
H. pylori-derived EVs were upregulated when compared with healthy controls. Stomach epithelial cells selectively targeting and taken up
H. pylori -derived EVs.
H. pylori-derived EVs enhanced in the gastric juices of gastric adenocarcinoma patients and promoted inflammation mainly via specific targeting of gastric epithelial cells [
60]. CagA was present in serum-derived exosomes in patients infected with cagA-positive
H. pylori has been reported. These exosomes may from gastric epithelial cells which inducibly expressing CagA secret exosomes, and then entered into circulation, transferring CagA to distant organs and tissues [
61]. Pan et al found association between
H.pylori-infected GC cells and macrophages through exosome. They also demonstrated that
H.pylori-induced exosomal MET educated tumor-associated macrophages to promote gastric cancer progression [
62]. Human T cell responses was inhibited by
H.pylori outer membrane vesicles via induction of monocyte cyclo-oxygenase-2 (COX-2) expression has been proved. The outer membrane of
H. pylori releases vesicles to modulate the immune system. Subsequent T cell proliferation was inhibited by PBMC significantly after addition of
H. pylori outer membrane vesicles in a COX-2 dependent manner. Expression of COX-2 was significantly induced by
H. pylori outer membrane vesicles which was inducing by the monocytes present and significantly increased levels of PGE2 and IL-10. These results suggest that
H. pylori outer membrane vesicles can suppress human T cell responses is not only through a direct effect on the T cells but also results from the induction of COX-2 expression in monocytes [
63].