ArticlePLoS pathogens2008
Sphingomyelin functions as a novel receptor for Helicobacter pylori VacA.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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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
63 citing papers in PubMed, 111 citations in OpenAlex.
- Review
- Bacterial Toxin Exploits Host Membrane Phospholipid as a Receptor for Binding, Entry, and Cytopathogenicity.Molecular microbiology · 2026Article
- A vicious cycle inducer in gastric pathogenesis: implication of Helicobacter pylori.Archives of microbiology · 2026Review
- Vacuolating Cytotoxin A (VacA) and Extracellular Vesicles inIranian journal of pathology · 2025Review
- Structural Analysis of Membrane-associated Forms of Helicobacter pylori VacA Toxin.Journal of molecular biology · 2024Article
- There Are No Insurmountable Barriers: Passage of theMembranes · 2023Review
- Restoration of mitochondrial structure and function withinAdvances in microbiology · 2023Article
- Review
- The role of human milk fats in shaping neonatal development and the early life gut microbiota.Microbiome research reports · 2023Review
- Cell lipid biology in infections: an overview.Frontiers in cellular and infection microbiology · 2023Review
- Gut microbiota mediates the alleviative effect of polar lipids-enriched milk fat globule membrane on obesity-induced glucose metabolism disorders in peripheral tissues in rat dams.International journal of obesity (2005) · 2022Article
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Functional Properties of Oligomeric and Monomeric Forms of Helicobacter pylori VacA Toxin.Infection and immunity · 2021Article
- Chronic in vivo exposure to Helicobacter pylori VacA: Assessing the efficacy of automated and long-term intragastric toxin infusion.Scientific reports · 2020Article
- Functional Properties of Helicobacter pylori VacA Toxin m1 and m2 Variants.Infection and immunity · 2020Article
- SHP2-Independent Tyrosine Dephosphorylation of Cortactin and Vinculin during Infection withEuropean journal of microbiology & immunology · 2020Article
- Actinoporins: From the Structure and Function to the Generation of Biotechnological and Therapeutic Tools.Biomolecules · 2020Review
- Helicobacter pylori-induced adrenomedullin modulates IFN-γ-producing T-cell responses and contributes to gastritis.Cell death & disease · 2020Article
- An Overview of Lipid Metabolism and Nonalcoholic Fatty Liver Disease.BioMed research international · 2020Review
- Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The vacuolating cytotoxin (VacA) of the gastric pathogen Helicobacter pylori binds and enters epithelial cells, ultimately resulting in cellular vacuolation. Several host factors have been reported to be important for VacA function, but none of these have been demonstrated to be essential for toxin binding to the plasma membrane. Thus, the identity of cell surface receptors critical for both toxin binding and function has remained elusive. Here, we identify VacA as the first bacterial virulence factor that exploits the important plasma membrane sphingolipid, sphingomyelin (SM), as a cellular receptor. Depletion of plasma membrane SM with sphingomyelinase inhibited VacA-mediated vacuolation and significantly reduced the sensitivity of HeLa cells, as well as several other cell lines, to VacA. Further analysis revealed that SM is critical for VacA interactions with the plasma membrane. Restoring plasma membrane SM in cells previously depleted of SM was sufficient to rescue both toxin vacuolation activity and plasma membrane binding. VacA association with detergent-resistant membranes was inhibited in cells pretreated with SMase C, indicating the importance of SM for VacA association with lipid raft microdomains. Finally, VacA bound to SM in an in vitro ELISA assay in a manner competitively inhibited by lysenin, a known SM-binding protein. Our results suggest a model where VacA may exploit the capacity of SM to preferentially partition into lipid rafts in order to access the raft-associated cellular machinery previously shown to be required for toxin entry into host cells.
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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.