Open AccessExternal membrane vesicles from Helicobacter pylori induce apoptosis in gastric epithelial cells
Author(s) -
Ayala Guadalupe,
Torres Luz,
Espinosa Magali,
FierrosZarate Geny,
Maldonado Vilma,
MeléndezZajgla Jorge
Publication year - 2006
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2006.00305.x
Subject(s) - helicobacter pylori , caga , biology , apoptosis , vesicle , bacterial outer membrane , virulence , pathogenicity island , microbiology and biotechnology , secretion , biochemistry , membrane , genetics , gene , escherichia coli
The Helicobacter pylori infection of gastric mucosa is one of the most common infectious diseases and is associated with a variety of clinical outcomes, including peptic ulcer disease and gastric cancer. Helicobacter pylori ‐induced damage to gastric mucosal cells is controlled by bacterial virulence factors, which include VacA and CagA. Outer membrane vesicles are constantly shed by the bacteria and can provide an additional mechanism for pathogenicity by releasing non‐secretable factors which can then interact with epithelial cells. The present report shows that external membrane vesicles are able to induce apoptosis not mediated by mitochondrial pathway in gastric (AGS) epithelial cells, as demonstrated by the lack of cytochrome c release with an activation of caspase 8 and 3. Apoptosis induced by these vesicles does not require a classic VacA + phenotype, as a negative strain with a truncated and therefore non‐secretable form of this protein can also induce cell death. These results should be taken into account in future studies of H. pylori pathogenicity in strains apparently VacA‐.