Evidence map›Paper›PMID 17101654›Full record

ArticleInfection and immunity2007

Identification of Helicobacter pylori genes that contribute to stomach colonization.

David N Baldwin, Benjamin Shepherd, Petra Kraemer, Michael K Hall, Laura K Sycuro, Delia M Pinto-Santini, Nina R Salama

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 142 citations in OpenAlex.

  1. Review
  2. Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026
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  6. Loureirin A is a narrow-spectrum antimicrobial agent againstAntimicrobial agents and chemotherapy · 2024
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  8. Role of nickel-regulated small RNA in modulation ofWorld journal of clinical cases · 2022
    Review
  9. Article
  10. Enhanced Fitness of a Helicobacter pyloriInfection and immunity · 2021
    Article
  11. Article
  12. Article
  13. A Mouse Model of Helicobacter pylori Infection.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Antibiotics (Basel, Switzerland) · 2020
    Article
  18. Review
  19. Antibiotic Resistance Results ofInternational journal of microbiology · 2020
    Article
  20. Article

18 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

7 authors at 2 institutions in 1 country.

David N BaldwinDivision of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Benjamin Shepherd
Petra Kraemer
Michael K Hall
Laura K Sycuro
Delia M Pinto-Santini
Nina R Salama
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

GENETIC REQUIREMENTS OF HELICOBACTER PYLORI INFECTIONR01AI054423 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Nina Salama · 2004 to 2026
$9.5M
NIAID NIH HHS AI054423NIAID NIH HHS R01 AI054423
6 · The paper itself

Abstract

Chronic infection of the human stomach by Helicobacter pylori leads to a variety of pathological sequelae, including peptic ulcer and gastric cancer, resulting in significant human morbidity and mortality. Several genes have been implicated in disease related to H. pylori infection, including the vacuolating cytotoxin and the cag pathogenicity island. Other factors important for the establishment and maintenance of infection include urease enzyme production, motility, iron uptake, and stress response. We utilized a C57BL/6 mouse infection model to query a collection of 2,400 transposon mutants in two different bacterial strain backgrounds for H. pylori genetic loci contributing to colonization of the stomach. Microarray-based tracking of transposon mutants allowed us to monitor the behavior of transposon insertions in 758 different gene loci. Of the loci measured, 223 (29%) had a predicted colonization defect. These included previously described H. pylori virulence genes, genes implicated in virulence in other pathogenic bacteria, and 81 hypothetical proteins. We have retested 10 previously uncharacterized candidate colonization gene loci by making independent null alleles and have confirmed their colonization phenotypes by using competition experiments and by determining the dose required for 50% infection. Of the genetic loci retested, 60% have strain-specific colonization defects, while 40% have phenotypes in both strain backgrounds for infection, highlighting the profound effect of H. pylori strain variation on the pathogenic potential of this organism.

Indexed as

Genes, BacterialAnimalsDisease Models, AnimalDNA, BacterialDNA Transposable ElementsFemaleGene DeletionGenome, BacterialHelicobacter InfectionsHelicobacter pyloriMiceMice, Inbred C57BLMutagenesis, InsertionalOligonucleotide Array Sequence AnalysisStomachVirulence FactorsDNA, BacterialDNA Transposable ElementsVirulence Factors

Identifiers

PMID17101654
PMCPMC1828534
OpenAlexW2108925945

What OpenQuestion holds

Textmetadata
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.