Evidence map›Paper›PMID 33245103›Full record

ArticleThe Journal of infectious diseases2021

Helicobacter pylori-Induced TLR9 Activation and Injury Are Associated With the Virulence-Associated Adhesin HopQ.

Samuel D R Dooyema, Uma S Krishna, John T Loh, Giovanni Suarez, Timothy L Cover, Richard M Peek

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of infectious diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Methylation Dynamics inMicroorganisms · 2026
    Article
  2. Review
  3. 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

6 authors at 1 institution in 1 country.

Samuel D R DooyemaDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Uma S KrishnaDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
John T LohDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Giovanni SuarezDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Timothy L CoverDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Richard M PeekDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Vanderbilt University Medical Center · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Role of Iron and B-Catenin Activation in Gastric CarcinogenesisP01CA116087 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2009 to 2026
$27.5M
H.Pylori Relationship to Digestive Diseases and CancerR01CA077955 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2003 to 2026
$9.7M
Helicobacter Pylori and Gastrointestinal BiologyR01DK058587 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PEEK, RICHARD M. · 2001 to 2024
$7.8M
Type IV Protein Secretion in Helicobacter pyloriR01AI118932 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI COVER, TIMOTHY L, OHI, MELANIE DIANE · 2016 to 2025
$6.7M
Chemical Biology of Infectious Diseases (CBID) Training ProgramT32AI112541 · NIAID · VANDERBILT UNIVERSITY · PI Eric P Skaar · 2015 to 2026
$4.0M
"Pathogenesis of Helicobacter pylori Infection"I01BX004447 · VA · VETERANS HEALTH ADMINISTRATION · PI TIMOTHY L COVER · 2019 to 2026
–
BLRD VA I01 BX004447NCI NIH HHS P01 CA116087NCI NIH HHS R01 CA077955NIAID NIH HHS R01 AI118932NIAID NIH HHS T32 AI112541NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK058587
6 · The paper itself

Abstract

Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma. The H. pylori cancer-associated cag pathogenicity island (cag-PAI) encodes a type IV secretion system (T4SS), which translocates microbial DNA and activates TLR9; however, most cag-PAI+-infected persons do not develop cancer and cag-PAI-independent regulators of pathogenesis, including strain-specific adhesins, remain understudied. We defined the relationships between H. pylori HopQ adhesin allelic type, gastric injury, and TLR9 activation. Type I hopQ alleles were significantly associated with magnitude of injury, cag-T4SS function, and TLR9 activation. Genetic deletion of hopQ significantly decreased H. pylori-induced TLR9 activation, implicating this adhesin in H. pylori-mediated disease.

Indexed as

Adhesins, BacterialHelicobacter InfectionsAntigens, BacterialBacterial ProteinsGenomic IslandsHelicobacter pyloriHumansToll-Like Receptor 9Type IV Secretion SystemsVirulenceAdhesins, BacterialAntigens, BacterialBacterial ProteinsTLR9 protein, humanToll-Like Receptor 9Type IV Secretion Systemsgastric cancerHelicobacter pyloriHopQsecretion systemsTLR9

Identifiers

PMID33245103
PMCPMC8280490
OpenAlexW3108947694

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.