Evidence map›Paper›PMID 22802346›Full record

ArticleInfection and immunity2012

Helicobacter pylori requires TlpD-driven chemotaxis to proliferate in the antrum.

Annah S Rolig, James Shanks, J Elliot Carter, Karen M Ottemann

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 72 citations in OpenAlex.

  1. ZnbioRxiv : the preprint server for biology · 2026
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  2. TheJournal of bacteriology · 2026
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  3. Structure and signaling mechanism ofbioRxiv : the preprint server for biology · 2026
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  4. Review
  5. World journal of gastroenterology · 2023
    Review
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  11. Plant-Based Polyphenols: Anti-Antioxidants (Basel, Switzerland) · 2022
    Review
  12. Article
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  14. Article
  15. TFF1 Induces Aggregation and Reduces Motility ofInternational journal of molecular sciences · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. What bacteria want.Environmental microbiology · 2018
    Review
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

4 authors at 2 institutions in 1 country.

Annah S RoligDepartment of Molecular, Cellular, and Developmental Biology, University of California, Santa Cruz, Santa Cruz, California, USA.
James Shanks
J Elliot Carter
Karen M Ottemann
University of California, Santa Cruz · USUniversity of South Alabama · US

Funding

Roles for Motility in Helicobactor pylori pathogenesisR01AI050000 · NIAID · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI OTTEMANN, KAREN M · 2002 to 2011
$3.6M
NIAID NIH HHS AI050000NIAID NIH HHS R01 AI050000
6 · The paper itself

Abstract

Different disease outcomes of Helicobacter pylori infection correlate with distinct inflammation patterns. These different inflammatory distributions may be initiated by differences in bacterial localization. One H. pylori property known to affect murine stomach localization is chemotaxis, the ability to move in response to chemical cues. In this report, we used nonchemotactic mutants (Che(-)) to analyze whether chemotaxis is required for initial colonization of particular stomach regions or for subsequent growth therein. We found that H. pylori behaves differently in the corpus, antrum, and corpus-antrum transition zone subregions of the stomach. This outcome suggests that these regions contain unique chemotactic signals. In the corpus, H. pylori utilizes chemotaxis for initial localization but not for subsequent growth. In contrast, in the antrum and the corpus-antrum transition zone, chemotaxis does not help initial colonization but does promote subsequent proliferation. To determine which chemoreceptor is responsible for the corpus-antrum phenotypes, we infected mice with strains lacking each chemoreceptor. Strains lacking TlpA, TlpB, or TlpC displayed only modest deviations from the wild-type phenotype, while strains lacking TlpD resembled the Che(-) mutant in their antral colonization defect and fared even worse than the Che(-) mutant in the corpus. Additional analysis showed that inflammation is worse in the antrum than in the corpus in both wild-type and Che(-) mutant infections. These results suggest that chemotaxis, specifically, that controlled by TlpD, is necessary for H. pylori to survive or grow in the environment of increased inflammation in the antrum.

Indexed as

AnimalsBacterial ProteinsChemotaxisEpitheliumFemaleHelicobacter InfectionsHelicobacter pyloriMiceMice, Inbred C57BLMutationPyloric AntrumStomach DiseasesBacterial Proteins

Identifiers

PMID22802346
PMCPMC3457577
OpenAlexW2108700884

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.