Evidence map›Paper›PMID 29696729›Full record

ArticleHelicobacter2018

Acid-regulated gene expression of Helicobacter pylori: Insight into acid protection and gastric colonization.

Elizabeth A Marcus, George Sachs, David R Scott

Abstract read
In one paragraph

Article in Helicobacter, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Methylation Dynamics inMicroorganisms · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. pH-dependent genotypic and phenotypic variability inApplied and environmental microbiology · 2025
    Article
  6. Article
  7. Frontiers in microbiology · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. TheJournal of bacteriology · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022
    Review
  16. Article
  17. World journal of gastroenterology · 2021
    Review
  18. Article
  19. Review
  20. Pathways of Gastric Carcinogenesis,International journal of molecular sciences · 2020
    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

3 authors at 1 institution in 1 country.

Elizabeth A MarcusDepartment of Pediatrics, David Geffen School of Medicine at UCLA and VA GLAHS, Los Angeles, CA, USA.
George SachsDepartment of Medicine, David Geffen School of Medicine at UCLA and VA GLAHS, Los Angeles, CA, USA.
David R ScottDepartment of Physiology, David Geffen School of Medicine at UCLA and VA GLAHS, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-1199-750X
University of California, Los Angeles · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
The role of ArsS in gastric infection by Helicobacter pyloriR01DK105156 · NIDDK · BRENTWOOD BIOMEDICAL RESEARCH INSTITUTE · PI MARCUS, ELIZABETH A. · 2015 to 2018
$1.1M
Mechanisms of gastric mucosal response to H. pylori infection at acidic pHK08DK100661 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARCUS, ELIZABETH A. · 2014 to 2017
$561k
Mechanisms of gastric injury by Helicbacter pyloriR03DK110579 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARCUS, ELIZABETH A. · 2017 to 2018
$126k
BLRD VA I01 BX001006NIDDK NIH HHS K08 DK100661NIDDK NIH HHS R01 DK105156NIDDK NIH HHS R03 DK110579
6 · The paper itself

Abstract

backgroundThe pathogen Helicobacter pylori encounters many stressors as it transits to and infects the gastric epithelium. Gastric acidity is the predominate stressor encountered by the bacterium during initial infection and establishment of persistent infection. H. pylori initiates a rapid response to acid to maintain intracellular pH and proton motive force appropriate for a neutralophile. However, acid sensing by H. pylori may also serve as a transcriptional trigger to increase the levels of other pathogenic factors needed to subvert host defenses such as acid acclimation, antioxidants, flagellar synthesis and assembly, and CagA secretion. MATERIALS AND

methodsHelicobacter pylori were acid challenged at pH 3.0, 4.5, 6.0 vs nonacidic pH for 4 hours in the presence of urea, followed by RNA-seq analysis and qPCR. Cytoplasmic pH was monitored under the same conditions.

resultsAbout 250 genes were induced, and an equal number were repressed at acidic pHs. Genes encoding for antioxidant proteins, flagellar structural proteins, particularly class 2 genes, T4SS/Cag-PAI, F

conclusionsThese results suggest that increasing extracellular or intracellular acidity or both are detected by the bacterium and serve as a signal to initiate increased production of protective and pathogenic factors needed to counter host defenses for persistent infection. These changes are dependent on degree of acidity and time of acid exposure, triggering a coordinated response to the environment required for colonization.

Indexed as

Gene Expression Regulation, BacterialAcidsAdaptation, PhysiologicalBacterial ProteinsCulture MediaHelicobacter pyloriHydrogen-Ion ConcentrationMultigene FamilyProteomeRNA, BacterialStomachTranscriptomeUreaseVirulence FactorsAcidsBacterial ProteinsCulture MediaProteomeRNA, BacterialUreaseVirulence Factorsacidic conditionHelicobacter pyloriRNA-seqtranscriptome

Identifiers

PMID29696729
PMCPMC5980792
OpenAlexW2800379528

What OpenQuestion holds

Textmetadata
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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.