External membrane vesicles from Helicobacter pylori induce apoptosis in gastric epithelial cells.
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-.
Ayala
Guadalupe
G
Centro de Investigación Sobre Enfermedades Infecciosas, Instituto Nacional de Salud Publica, Cuernavaca, México.
Torres
Luz
L
Espinosa
Magali
M
Fierros-Zarate
Geny
G
Maldonado
Vilma
V
Meléndez-Zajgla
Jorge
J
D017209:Apoptosis; D001426:Bacterial Proteins / Q000378:metabolism; D045744:Cell Line, Tumor; D002462:Cell Membrane / Q000648:ultrastructure*; D017077:Culture Media, Conditioned; D004847:Epithelial Cells / Q000382:microbiology / Q000502:physiology*; D005753:Gastric Mucosa / Q000166:cytology / Q000382:microbiology / Q000502:physiology*; D016480:Helicobacter pylori / Q000472:pathogenicity* / Q000648:ultrastructure; D006801:Humans; D014774:Virulence
D001426:Bacterial Proteins; D017077:Culture Media, Conditioned; C074689:VacA protein, Helicobacter pylori