Evidence map›Paper›PMID 12117971›Full record

ArticleInfection and immunity2002

Helicobacter pylori-induced activation of human endothelial cells.

M Innocenti, A-C Thoreson, R L Ferrero, E Strömberg, I Bölin, L Eriksson, A-M Svennerholm, M Quiding-Järbrink

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
9.0field-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

28 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
  2. Review
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Frontiers in medicine · 2020
    Article
  10. Article
  11. Hepatic Encephalopathy and Helicobacter pylori.Digestive diseases and sciences · 2018
    Article
  12. Frontiers in cellular and infection microbiology · 2018
    Article
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

M InnocentiDepartment of Medical Microbiology and Immunology, Sahlgrenska Academy at Göteborg University, Sweden. mikael.innocenti@rheuma.gu.se
A-C Thoreson
R L Ferrero
E Strömberg
I Bölin
L Eriksson
A-M Svennerholm
M Quiding-Järbrink
University of Gothenburg · SEInstitut Pasteur · FRSwedish Institute · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori infection causes active chronic inflammation with a continuous recruitment of neutrophils to the inflamed gastric mucosa. To evaluate the role of endothelial cells in this process, we have examined adhesion molecule expression and chemokine and cytokine production from human umbilical vein endothelial cells stimulated with well-characterized H. pylori strains as well as purified proteins. Our results indicate that endothelial cells actively contribute to neutrophil recruitment, since stimulation with H. pylori bacteria induced upregulation of the adhesion molecules VCAM-1, ICAM-1, and E-selectin as well as the chemokines interleukin 8 (IL-8) and growth-related oncogene alpha (GRO-alpha) and the cytokine IL-6. However, there were large variations in the ability of the different H. pylori strains to stimulate endothelial cells. These interstrain variations were seen irrespective of whether the strains had been isolated from patients with duodenal ulcer disease or asymptomatic carriers and were not solely related to the expression of known virulence factors, such as the cytotoxin-associated gene pathogenicity island, vacuolating toxin A, and Lewis blood group antigens. In addition, one or several unidentified proteins which act via NF-kappaB activation seem to induce endothelial cell activation. In conclusion, human endothelial cells produce neutrophil-recruiting factors and show increased adhesion molecule expression after stimulation with certain H. pylori strains. These effects probably contribute to the continuous recruitment of neutrophils to H. pylori-infected gastric mucosa and may also contribute to tissue damage and ulcer formation.

Indexed as

Intercellular Signaling Peptides and ProteinsAdultBacterial AdhesionBacterial ProteinsCells, CulturedChemokine CCL5Chemokine CXCL1Chemokine CXCL10Chemokines, CXCChemotactic FactorsEndothelium, VascularE-SelectinGranulocyte-Macrophage Colony-Stimulating FactorGrowth SubstancesHelicobacter pyloriHumansBacterial ProteinsChemokine CCL5Chemokine CXCL1Chemokine CXCL10Chemokines, CXCChemotactic FactorsCXCL1 protein, humanE-SelectinGranulocyte-Macrophage Colony-Stimulating FactorGrowth SubstancesIntercellular Adhesion Molecule-1Intercellular Signaling Peptides and ProteinsInterleukin-6Interleukin-8NF-kappa BVascular Cell Adhesion Molecule-1

Identifiers

PMID12117971
PMCPMC128191
OpenAlexW2103765645

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.