Evidence map›Paper›PMID 15972508›Full record

ArticleInfection and immunity2005

Impact of Helicobacter pylori virulence factors and compounds on activation and maturation of human dendritic cells.

Katharina Kranzer, Liane Söllner, Michael Aigner, Norbert Lehn, Ludwig Deml, Michael Rehli, Wulf Schneider-Brachert

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.2field-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

29 citing papers in PubMed, 71 citations in OpenAlex.

  1. Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026
    Review
  2. Role of Gastric Microorganisms Other thanBioMed research international · 2022
    Review
  3. Immunological Perspective:Mediators of inflammation · 2022
    Review
  4. Article
  5. T Cell Cytokines Impact Epithelial Cell Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020
    Review
  6. The Role of Gastric Mucosal Immunity in Gastric Diseases.Journal of immunology research · 2020
    Review
  7. Article
  8. Article
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  10. Article
  11. Review
  12. Article
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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

7 authors at 1 institution in 1 country.

Katharina KranzerInstitute for Medical Microbiology and Hygiene, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany.
Liane Söllner
Michael Aigner
Norbert Lehn
Ludwig Deml
Michael Rehli
Wulf Schneider-Brachert
University of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, we and others have shown that Helicobacter pylori induces dendritic cell (DC) activation and maturation. However, the impact of virulence factors on the interplay between DCs and H. pylori remains elusive. Therefore, we investigated the contribution of cag pathogenicity island (PAI) and VacA status on cytokine release and up-regulation of costimulatory molecules in H. pylori-treated DCs. In addition, to characterize the stimulatory capacity of H. pylori compounds in more detail, we studied the effect of formalin-inactivated and sonicated H. pylori, as well as secreted H. pylori molecules, on DCs. Incubation of DCs with viable or formalin-inactivated H. pylori induced comparable secretion of interleukin-6 (IL-6), IL-8, IL-10, IL-12, IL-1beta, and tumor necrosis factor (TNF). In contrast, IL-12 and IL-1beta release was significantly reduced in DCs treated with sonicated bacteria and secreted bacterial molecules. Treatment of sonicated H. pylori preparations with polymyxin B resulted in a significant reduction of IL-8 and IL-6 secretion, suggesting that H. pylori-derived lipopolysaccharide at least partially contributes to activation of immature DCs. In addition, the capacity of H. pylori-pulsed DCs to activate allogeneic T cells was not affected by cag PAI and VacA. Pretreatment of DC with cytochalasin D significantly inhibited secretion of IL-12, IL-1beta, and TNF, indicating that phagocytosis of H. pylori contributes to maximal activation of DCs. Taken together, our results suggest that DC activation and maturation, as well as DC-mediated T-cell activation, are independent of the cag PAI and VacA status of H. pylori.

Indexed as

Antigens, BacterialBacterial ProteinsCells, CulturedCytokinesDendritic CellsGenomic IslandsHelicobacter pyloriHumansLipopolysaccharidesLymphocyte ActivationMembrane GlycoproteinsPhagocytosisReceptors, Cell SurfaceT-LymphocytesToll-Like ReceptorsVirulence FactorsAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriCytokinesLipopolysaccharidesMembrane GlycoproteinsReceptors, Cell SurfaceToll-Like ReceptorsVacA protein, Helicobacter pyloriVirulence Factors

Identifiers

PMID15972508
PMCPMC1168582
OpenAlexW2001858701

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.