Evidence map›Paper›PMID 25033386›Full record

ArticlePLoS pathogens2014

Motility and chemotaxis mediate the preferential colonization of gastric injury sites by Helicobacter pylori.

Eitaro Aihara, Chet Closson, Andrea L Matthis, Michael A Schumacher, Amy C Engevik, Yana Zavros, Karen M Ottemann, Marshall H Montrose

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Characterization of aFrontiers in cellular and infection microbiology · 2026
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  3. Acquired tick resistance inInfection and immunity · 2025
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  4. Review
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  6. Article
  7. A critical review onFrontiers in cellular and infection microbiology · 2025
    Review
  8. Reassessing the Standard Chemotaxis Framework for Understanding Biased Migration inAnnual review of chemical and biomolecular engineering · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. World journal of gastroenterology · 2023
    Review
  13. Bacterial chemotaxis in human diseases.Trends in microbiology · 2023
    Review
  14. Review
  15. Review
  16. Review
  17. Hesperetin Inhibits Expression of Virulence Factors and Growth ofInternational journal of molecular sciences · 2021
    Article
  18. Article
  19. International journal of molecular sciences · 2021
    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

8 authors at 2 institutions in 1 country.

Eitaro AiharaDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, United States of America.
Chet ClossonDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, United States of America.
Andrea L MatthisDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, United States of America.
Michael A SchumacherDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, United States of America.
Amy C EngevikDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, United States of America.
Yana ZavrosDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, United States of America.
Karen M OttemannDepartment of Microbiology and Environmental Toxicology, University of California at Santa Cruz, Santa Cruz, California, United States of America.
Marshall H MontroseDepartment of Molecular and Cellular Physiology, University of Cincinnati, Cincinnati, Ohio, United States of America.
University of Cincinnati · USUniversity of California, Santa Cruz · US

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
SENSING PH AT THE GASTRIC SURFACER01DK054940 · NIDDK · UNIVERSITY OF CINCINNATI · PI MONTROSE, MARSHALL H · 1999 to 2013
$4.3M
The role of Hedgehog Signaling in gastric tissue repair and regenerationR01DK083402 · NIDDK · UNIVERSITY OF CINCINNATI · PI ZAVROS, YANA · 2011 to 2019
$3.7M
NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK054940NIDDK NIH HHS R01 DK083402
6 · The paper itself

Abstract

Helicobacter pylori (H. pylori) is a pathogen contributing to peptic inflammation, ulceration, and cancer. A crucial step in the pathogenic sequence is when the bacterium first interacts with gastric tissue, an event that is poorly understood in vivo. We have shown that the luminal space adjacent to gastric epithelial damage is a microenvironment, and we hypothesized that this microenvironment might enhance H. pylori colonization. Inoculation with 106 H. pylori (wild-type Sydney Strain 1, SS1) significantly delayed healing of acetic-acid induced ulcers at Day 1, 7 and 30 post-inoculation, and wild-type SS1 preferentially colonized the ulcerated area compared to uninjured gastric tissue in the same animal at all time points. Gastric resident Lactobacillus spp. did not preferentially colonize ulcerated tissue. To determine whether bacterial motility and chemotaxis are important to ulcer healing and colonization, we analyzed isogenic H. pylori mutants defective in motility (ΔmotB) or chemotaxis (ΔcheY). ΔmotB (10(6)) failed to colonize ulcerated or healthy stomach tissue. ΔcheY (10(6)) colonized both tissues, but without preferential colonization of ulcerated tissue. However, ΔcheY did modestly delay ulcer healing, suggesting that chemotaxis is not required for this process. We used two-photon microscopy to induce microscopic epithelial lesions in vivo, and evaluated accumulation of fluorescently labeled H. pylori at gastric damage sites in the time frame of minutes instead of days. By 5 min after inducing damage, H. pylori SS1 preferentially accumulated at the site of damage and inhibited gastric epithelial restitution. H. pylori ΔcheY modestly accumulated at the gastric surface and inhibited restitution, but did not preferentially accumulate at the injury site. H. pylori ΔmotB neither accumulated at the surface nor inhibited restitution. We conclude that bacterial chemosensing and motility rapidly promote H. pylori colonization of injury sites, and thereby biases the injured tissue towards sustained gastric damage.

Indexed as

Gastric MucosaAcetic AcidAnimalsHelicobacter InfectionsHelicobacter pyloriIndicators and ReagentsMiceStomach UlcerAcetic AcidIndicators and Reagents

Identifiers

PMID25033386
PMCPMC4102597
OpenAlexW2086829247

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.