ArticleThe Journal of clinical investigation2001
The Helicobacter pylori VacA toxin is a urea permease that promotes urea diffusion across epithelia.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 105 citations in OpenAlex.
- Review
- Bacteria and Carcinogenesis and the Management of Cancer: A Narrative Review.Pathogens (Basel, Switzerland) · 2025Review
- Vacuolating Cytotoxin A (VacA) and Extracellular Vesicles inIranian journal of pathology · 2025Review
- Helicobacter pylori infection and Parkinson's Disease: etiology, pathogenesis and levodopa bioavailability.Immunity & ageing : I & A · 2024Review
- There Are No Insurmountable Barriers: Passage of theMembranes · 2023Review
- Inflammation and Gastric Cancer.Diseases (Basel, Switzerland) · 2022Review
- Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022Review
- The impact of the human microbiome in tumorigenesis, cancer progression, and biotherapeutic development.BMC microbiology · 2022Review
- Review
- Infectious Aetiology of Marginal Zone Lymphoma and Role of Anti-Infective Therapy.Mediterranean journal of hematology and infectious diseases · 2016Review
- Expression of the Helicobacter pylori virulence factor vacuolating cytotoxin A (vacA) is influenced by a potential stem-loop structure in the 5' untranslated region of the transcript.Molecular microbiology · 2015Article
- Tight junction disruption: Helicobacter pylori and dysregulation of the gastric mucosal barrier.World journal of gastroenterology · 2015Review
- Exploring alternative treatments for Helicobacter pylori infection.World journal of gastroenterology · 2014Review
- Transcriptional profiling of gastric epithelial cells infected with wild type or arginase-deficient Helicobacter pylori.BMC microbiology · 2012Article
- Remodeling the host environment: modulation of the gastric epithelium by the Helicobacter pylori vacuolating toxin (VacA).Frontiers in cellular and infection microbiology · 2012Review
- Multifactorial etiology of gastric cancer.Methods in molecular biology (Clifton, N.J.) · 2012Review
- Helicobacter pylori perturbs iron trafficking in the epithelium to grow on the cell surface.PLoS pathogens · 2011Article
- Change is good: variations in common biological mechanisms in the epsilonproteobacterial genera Campylobacter and Helicobacter.Microbiology and molecular biology reviews : MMBR · 2011Review
- Role of innate immunity in Helicobacter pylori-induced gastric malignancy.Physiological reviews · 2010Review
- the versatility of the Helicobacter pylori vacuolating cytotoxin vacA in signal transduction and molecular crosstalk.Toxins · 2010Article
Corrections and comments
- Commented on by
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Urease and the cytotoxin VacA are two major virulence factors of the human pathogen Helicobacter pylori, which is responsible for severe gastroduodenal diseases. Diffusion of urea, the substrate of urease, into the stomach is critically required for the survival of infecting H. pylori. We now show that VacA increases the transepithelial flux of urea across model epithelia by inducing an unsaturable permeation pathway. This transcellular pathway is selective, as it conducts thiourea, but not glycerol and mannitol, demonstrating that it is not due to a loosening of intercellular junctions. Experiments performed with different cell lines, grown in a nonpolarized state, confirm that VacA permeabilizes the cell plasma membrane to urea. Inhibition studies indicate that transmembrane pores formed by VacA act as passive urea transporters. Thus, their inhibition by the anion channel blocker 5-nitro-2-(3-phenylpropylamino) benzoic acid significantly decreases toxin-induced urea fluxes in both polarized and nonpolarized cells. Moreover, phloretin, a well-known inhibitor of eukaryotic urea transporters, blocks VacA-mediated urea and ion transport and the toxin's main biologic effects. These data show that VacA behaves as a low-pH activated, passive urea transporter potentially capable of permeabilizing the gastric epithelium to urea. This opens the novel possibility that in vivo VacA may favor H. pylori infectivity by optimizing urease activity.
Indexed as
Identifiers
What OpenQuestion holds
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.