Evidence map›Paper›PMID 19412339›Full record

ArticlePLoS pathogens2009

Helicobacter pylori usurps cell polarity to turn the cell surface into a replicative niche.

Shumin Tan, Lucy S Tompkins, Manuel R Amieva

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
14.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

95 citing papers in PubMed, 150 citations in OpenAlex.

  1. Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026
    Review
  2. Characterization ofFrontiers in microbiology · 2026
    Article
  3. Infection byHaematologica · 2024
    Article
  4. Destruction of the brush border byFrontiers in microbiology · 2024
    Article
  5. Biofilm ofAntibiotics (Basel, Switzerland) · 2023
    Review
  6. Article
  7. International journal of molecular sciences · 2022
    Review
  8. Article
  9. Enhanced Fitness of a Helicobacter pyloriInfection and immunity · 2021
    Article
  10. Cytokine Profile of CCR6Sovremennye tekhnologii v meditsine · 2021
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Helicobacter pylori: preying on SIVA for survival in the stomach.The Journal of clinical investigation · 2020
    Article
  16. CagA-ASPP2 complex mediates loss of cell polarity and favorsProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Article

35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Shumin TanDepartment of Microbiology and Immunology, Stanford University, Stanford, CA, USA.
Lucy S Tompkins
Manuel R Amieva
Stanford University · US

Funding

GENETICS AND CELLULAR BASIS OF H PYLORI PATHOGENESISR01AI038459 · NIAID · STANFORD UNIVERSITY · PI TOMPKINS, LUCY STUART · 1996 to 2010
$4.0M
Helicobacter Host Interactions in Animal ModelsR01CA092229 · NCI · STANFORD UNIVERSITY · PI AMIEVA, MANUEL R · 2001 to 2009
$2.6M
NCI NIH HHS R01 CA092229NCI NIH HHS R01 CA92229NIAID NIH HHS R01 AI038459
6 · The paper itself

Abstract

Helicobacter pylori (Hp) intimately interacts with the gastric epithelial surface and translocates the virulence factor CagA into host cells in a contact-dependent manner. To study how Hp benefits from interacting with the cell surface, we developed live-cell microscopy methods to follow the fate of individual bacteria on the cell surface and find that Hp is able to replicate and form microcolonies directly over the intercellular junctions. On polarized epithelia, Hp is able to grow directly on the apical cell surface in conditions that do not support the growth of free-swimming bacteria. In contrast, mutants in CagA delivery are defective in colonization of the apical cell surface. Hp perturbs the polarized epithelium in a highly localized manner, since wild-type Hp does not rescue the growth defect of the CagA-deficient mutants upon co-infection. CagA's ability to disrupt host cell polarity is a key factor in enabling colonization of the apical cell surface by Hp, as disruption of the atypical protein kinase C/Par1b polarity pathway leads to rescue of the mutant growth defect during apical infection, and CagA-deficient mutants are able to colonize the polarized epithelium when given access to the basolateral cell surface. Our study establishes the cell surface as a replicative niche and the importance of CagA and its effects on host cell polarity for this purpose.

Indexed as

Bacterial AdhesionCell PolarityAnimalsAntigens, BacterialBacterial ProteinsCell LineCell MembraneDogsHelicobacter pyloriIntercellular JunctionsMicroscopy, FluorescenceMutationAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pylori

Identifiers

PMID19412339
PMCPMC2669173
OpenAlexW2054901782

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.