Evidence map›Paper›PMID 20523725›Full record

ArticlePloS one2010

Helicobacter pylori impairs murine dendritic cell responses to infection.

Ya-Hui Wang, Jean-Pierre Gorvel, Yen-Ting Chu, Jiunn-Jong Wu, Huan-Yao Lei

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
8.0field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Debate on the relationship betweenFrontiers in microbiology · 2024
    Pooled it
  2. Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026
    Review
  3. World journal of gastroenterology · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. The immunoregulatory role of helper T cells inFrontiers in immunology · 2025
    Review
  8. Strategies ofFrontiers in cellular and infection microbiology · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Intracellular Presence ofMicroorganisms · 2021
    Article
  16. Review
  17. Review
  18. Article
  19. Bacteria Exploit Autophagy For Their Own Benefit.Infection and drug resistance · 2019
    Review
  20. 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

5 authors at 2 institutions in 2 countries.

Ya-Hui WangInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan, Republic of China.
Jean-Pierre Gorvel
Yen-Ting Chu
Jiunn-Jong Wu
Huan-Yao Lei
National Cheng Kung University · TWAix-Marseille Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHelicobacter pylori, a human pathogen associated with chronic gastritis, peptic ulcer and gastric malignancies, is generally viewed as an extracellular microorganism. Here, we show that H. pylori replicates in murine bone marrow derived-dendritic cells (BMDCs) within autophagosomes. METHODOLOGY/PRINCIPAL

findingsA 10-fold increase of CFU is found between 2 h and 6 h p.i. in H. pylori-infected BMDCs. Autophagy is induced around the bacterium and participates at late time points of infection for the clearance of intracellular H. pylori. As a consequence of infection, LC3, LAMP1 and MHC class II molecules are retained within the H. pylori-containing vacuoles and export of MHC class II molecules to cell surface is blocked. However, formalin-fixed H. pylori still maintain this inhibitory activity in BMDC derived from wild type mice, but not in from either TLR4 or TLR2-deficient mice, suggesting the involvement of H. pylori-LPS in this process. TNF-alpha, IL-6 and IL-10 expression was also modulated upon infection showing a TLR2-specific dependent IL-10 secretion. No IL-12 was detected favoring the hypothesis of a down modulation of DC functions during H. pylori infection. Furthermore, antigen-specific T cells proliferation was also impaired upon infection. CONCLUSIONS/SIGNIFICANCE: H. pylori can infect and replicate in BMDCs and thereby affects DC-mediated immune responses. The implication of this new finding is discussed for the biological life cycle of H. pylori in the host.

Indexed as

AnimalsAutophagyBiological TransportBone Marrow CellsCell MembraneCell ProliferationCytokinesDendritic CellsFemaleHelicobacter InfectionsHelicobacter pyloriHistocompatibility Antigens Class IIMiceMice, Inbred C57BLToll-Like Receptor 2Toll-Like Receptor 4CytokinesHistocompatibility Antigens Class IITlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID20523725
PMCPMC2877707
OpenAlexW2012264087

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.