Evidence map›Paper›PMID 12060779›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Rapid genetic analysis of Helicobacter pylori gastric mucosal colonization in suckling mice.

Betty P Guo, John J Mekalanos

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Enhanced Fitness of a Helicobacter pyloriInfection and immunity · 2021
    Article
  4. Article
  5. Article
  6. Review
  7. An outer membrane channel protein of Mycobacterium tuberculosis with exotoxin activity.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Overview: Helicobacter pylori and extragastric disease.International journal of hematology · 2006
    Review
  17. Review
  18. Article
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Betty P GuoDepartment of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Avenue, Armenise 408, Boston, MA 02115.
John J Mekalanos
Harvard University · US

Funding

COORDINATE REGULATION OF BACTERIAL VIRULENCE FACTORSR01AI026289 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI MEKALANOS, JOHN JOSEPH · 1988 to 2018
$8.3M
NIAID NIH HHS AI 26289NIAID NIH HHS R01 AI026289
6 · The paper itself

Abstract

Previously described animal models for Helicobacter pylori infection have been limited by cumbersome host requirements (e.g., germ-free conditions or unusual species) or are applicable to only special subsets of H. pylori strains (e.g., fresh clinical isolates or animal-adapted derivatives). Here, we report that 5- to 6-day-old outbred CD-1 (ICR) suckling mice support 24-h colonization of all H. pylori strains tested (SS1, 26695 SmR-1, 43504 SmR-1, and G27 SmR-1), including lab-passaged strains that cannot be adapted for colonization of adult animals. Total colony-forming units (cfu) recovered from infection with lab-passaged strains did not differ from those with mouse-adapted SS1. We also tested this model's ability to detect colonization defects in strains carrying mutations in known virulence genes by coinfecting with wild-type H. pylori and measuring differential recovery. This competition assay identified colonization defects in several classes of known attenuated mutants, including those defective in acid resistance (ureA), metabolism (frdA), motility (motB), and chemotaxis (cheY). A mutant defective in copA (copper transporting P-type ATPase) is nonattenuated in adult and infant mice. Possibly because of the limited duration of infection, our model did not identify defects in vacuolating cytotoxin (vacA) or gamma-glutamyltranspeptidase (ggt) as attenuating, in contrast to results from other animal models. We also identified a new virulence gene (HP0507) encoding a conserved hypothetical protein, which is important for colonization in our model. The suckling mouse model offers a rapid method to identify colonization defects in any H. pylori strain and may have utility as a new tool for studying immunity to primary infection.

Indexed as

AgingAmino Acid SequenceAnimalsAnimals, SucklingDNA PrimersGastric MucosaHelicobacter pyloriHumansMiceMice, Inbred ICRMolecular Sequence DataMutagenesisMutationSequence AlignmentSequence Homology, Amino AcidDNA Primers

Identifiers

PMID12060779
PMCPMC123071
OpenAlexW2113992147

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.