Journal
AUTOPHAGY
Volume 5, Issue 3, Pages 370-379Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.5.3.7663
Keywords
VacA; H. pylori; autophagy
Categories
Funding
- ASM International Studentship
- CIHR [MOP-86619]
- Crohn's and Colitis Foundation of Canada
- Canadian Association of Gastroenterology/CIHR/Abbott
- NIH [R01 AI45928]
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Host cell responses to Helicobacter pylori infection are complex and incompletely understood. Here, we report that autophagy is induced within human-derived gastric epithelial cells (AGS) in response to H. pylori infection. These autophagosomes were distinct and different from the large vacuoles induced during H. pylori infection. Autophagosomes were detected by transmission electron microscopy, conversion of LC3-I to LC3-II, GFP-LC3 recruitment to autophagosomes, and depended on Atg5 and Atg12. The induction of autophagy depended on the vacuolating cytotoxin (VacA) and, moreover, VaCA was sufficient to induce autophagosome formation. The channel-forming activity of VacA was necessary for inducing autophagy. Intracellular VacA partially co-localized with GFP-LC3, indicating that the toxin associates with autophagosomes. The inhibition of autophagy increased the stability of intracellular VacA, which in turn resulted in enhanced toxin-mediated cellular vacuolation. These findings suggest that the induction of autophagy by VaCA may represent a host mechanism to limit toxin-induced cellular damage.
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