Evidence map›Paper›PMID 21589900›Full record

ArticlePLoS pathogens2011

Helicobacter pylori perturbs iron trafficking in the epithelium to grow on the cell surface.

Shumin Tan, Jennifer M Noto, Judith Romero-Gallo, Richard M Peek, Manuel R Amieva

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
13.6field-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

102 citing papers in PubMed, 165 citations in OpenAlex.

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  12. Destruction of the brush border byFrontiers in microbiology · 2024
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  15. International journal of molecular sciences · 2022
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  16. Role of nickel-regulated small RNA in modulation ofWorld journal of clinical cases · 2022
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  19. New Advances in Nano-Drug Delivery Systems:Frontiers in oncology · 2022
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  20. Immunological Perspective:Mediators of inflammation · 2022
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42 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

5 authors at 2 institutions in 1 country.

Shumin TanDepartment of Microbiology and Immunology, Stanford University, Stanford, California, United States of America.
Jennifer M Noto
Judith Romero-Gallo
Richard M Peek
Manuel R Amieva
Vanderbilt University · USStanford University · US

Funding

H.Pylori Relationship to Digestive Diseases and CancerR01CA077955 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2003 to 2026
$9.7M
Helicobacter Pylori and Gastrointestinal BiologyR01DK058587 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PEEK, RICHARD M. · 2001 to 2024
$7.8M
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
H PYLORI RELATIONSHIP TO DIGESTIVE DISEASES AND CANCERR29CA077955 · NCI · VANDERBILT UNIVERSITY · PI PEEK, RICHARD M · 1997 to 2001
$294k
NCI NIH HHS CA116837NCI NIH HHS CA77955NCI NIH HHS CA92229NCI NIH HHS R01 CA077955NCI NIH HHS R01 CA092229NCI NIH HHS R29 CA077955NIAID NIH HHS AI038459NIAID NIH HHS R01 AI038459NIDDK NIH HHS DK58587NIDDK NIH HHS R01 DK058587
6 · The paper itself

Abstract

Helicobacter pylori (Hp) injects the CagA effector protein into host epithelial cells and induces growth factor-like signaling, perturbs cell-cell junctions, and alters host cell polarity. This enables Hp to grow as microcolonies adhered to the host cell surface even in conditions that do not support growth of free-swimming bacteria. We hypothesized that CagA alters host cell physiology to allow Hp to obtain specific nutrients from or across the epithelial barrier. Using a polarized epithelium model system, we find that isogenic ΔcagA mutants are defective in cell surface microcolony formation, but exogenous addition of iron to the apical medium partially rescues this defect, suggesting that one of CagA's effects on host cells is to facilitate iron acquisition from the host. Hp adhered to the apical epithelial surface increase basolateral uptake of transferrin and induce its transcytosis in a CagA-dependent manner. Both CagA and VacA contribute to the perturbation of transferrin recycling, since VacA is involved in apical mislocalization of the transferrin receptor to sites of bacterial attachment. To determine if the transferrin recycling pathway is involved in Hp colonization of the cell surface, we silenced transferrin receptor expression during infection. This resulted in a reduced ability of Hp to colonize the polarized epithelium. To test whether CagA is important in promoting iron acquisition in vivo, we compared colonization of Hp in iron-replete vs. iron-deficient Mongolian gerbils. While wild type Hp and ΔcagA mutants colonized iron-replete gerbils at similar levels, ΔcagA mutants are markedly impaired in colonizing iron-deficient gerbils. Our study indicates that CagA and VacA act in concert to usurp the polarized process of host cell iron uptake, allowing Hp to use the cell surface as a replicative niche.

Indexed as

Adaptation, PhysiologicalAnimalsAntigens, BacterialBacterial AdhesionBacterial ProteinsCaco-2 CellsCell LineCell MembraneCell PolarityDogsDown-RegulationEpitheliumGastric MucosaGerbillinaeHelicobacter InfectionsHelicobacter pyloriAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriIronReceptors, TransferrinTransferrinVacA protein, Helicobacter pylori

Identifiers

PMID21589900
PMCPMC3093365
OpenAlexW2079054594

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.