ArticleInfection and immunity2006
Helicobacter pylori VacA toxin promotes bacterial intracellular survival in gastric epithelial cells.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 111 citations in OpenAlex.
- Internalization ofAnnals of medicine · 2026Review
- The role of toxin-antitoxin systems inJournal of bacteriology · 2026Review
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Autophagy-driven modulation of stem cell dynamics inVirulence · 2025Article
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- The spectrum of lysosomal stress and damage responses: from mechanosensing to inflammation.EMBO reports · 2025Review
- Vacuolating Cytotoxin A (VacA) and Extracellular Vesicles inIranian journal of pathology · 2025Review
- Legionella pneumophila exploits the endo-lysosomal network for phagosome biogenesis by co-opting SUMOylated Rab7.PLoS pathogens · 2024Article
- Implications of lncRNAs inFrontiers in cellular and infection microbiology · 2024Review
- There Are No Insurmountable Barriers: Passage of theMembranes · 2023Review
- Article
- Review
- Pathogenomics of Helicobacter pylori.Current topics in microbiology and immunology · 2023Review
- Article
- An Overview of Autophagy inFrontiers in cellular and infection microbiology · 2022Review
- Review
- Endolysosomal TRPMLs in Cancer.Biomolecules · 2021Review
- Biofilm Formation as a Complex Result of Virulence and Adaptive Responses ofPathogens (Basel, Switzerland) · 2020Review
- High expression of Helicobacter pylori VapD in both the intracellular environment and biopsies from gastric patients with severity.PloS one · 2020Article
- Endomembrane Tension and Trafficking.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
Helicobacter pylori colonizes the gastric epithelium of at least 50% of the world's human population, playing a causative role in the development of chronic gastritis, peptic ulcers, and gastric adenocarcinoma. Current evidence indicates that H. pylori can invade epithelial cells in the gastric mucosa. However, relatively little is known about the biology of H. pylori invasion and survival in host cells. Here, we analyze both the nature of and the mechanisms responsible for the formation of H. pylori's intracellular niche. We show that in AGS cells infected with H. pylori, bacterium-containing vacuoles originate through the fusion of late endocytic organelles. This process is mediated by the VacA-dependent retention of the small GTPase Rab7. In addition, functional interactions between Rab7 and its downstream effector, Rab-interacting lysosomal protein (RILP), are necessary for the formation of the bacterial compartment since expression of mutant forms of RILP or Rab7 that fail to bind each other impaired the formation of this unique bacterial niche. Moreover, the VacA-mediated sequestration of active Rab7 disrupts the full maturation of vacuoles as assessed by the lack of both colocalization with cathepsin D and degradation of internalized cargo in the H. pylori-containing vacuole. Based on these findings, we propose that the VacA-dependent isolation of the H. pylori-containing vacuole from bactericidal components of the lysosomal pathway promotes bacterial survival and contributes to the persistence of infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.