Evidence map›Paper›PMID 24421041›Full record

ArticleInfection and immunity2014

Helicobacter pylori membrane vesicles stimulate innate pro- and anti-inflammatory responses and induce apoptosis in Jurkat T cells.

Jody Winter, Darren Letley, Joanne Rhead, John Atherton, Karen Robinson

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

61 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Beyond the Stomach: Exploring the Role ofExpert reviews in molecular medicine · 2026
    Review
  3. Article
  4. Bacterial Outer Membrane Vesicles in Potentiating Cancer Vaccines: Progress and Prospects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. UnravelingVaccines · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Opportunities forMicroorganisms · 2024
    Review
  19. Review
  20. Programmed cell death inFrontiers in cellular and infection microbiology · 2024
    Review

1 more citing papers are in PubMed but not listed here.

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 1 country.

Jody WinterNottingham Digestive Diseases Centre Biomedical Research Unit, School of Clinical Sciences, Centre for Biomolecular Sciences, The University of Nottingham, Nottingham, United Kingdom.
Darren Letley
Joanne Rhead
John Atherton
Karen Robinson
NIHR Nottingham Digestive Diseases Biomedical Research Unit · GBUniversity of Nottingham · GB

Funding

Cancer Research UK C8968/A11204Medical Research Council G0601170
6 · The paper itself

Abstract

Persistent Helicobacter pylori infection induces chronic inflammation in the human gastric mucosa, which is associated with development of peptic ulceration, gastric atrophy, and gastric adenocarcinoma. It has been postulated that secretion of immunomodulatory molecules by H. pylori facilitates bacterial persistence, and membrane vesicles (MV), which have the potential to cross the gastric epithelial barrier, may mediate delivery of these molecules to host immune cells. However, bacterial MV effects on human immune cells remain largely uncharacterized to date. In the present study, we investigated the immunomodulatory effects of H. pylori MV with and without the vacuolating cytotoxin, VacA, which inhibits human T cell activity. We show a high degree of variability in the toxin content of vesicles between two H. pylori strains (SS1 and 60190). Vesicles from the more toxigenic 60190 strain contain more VacA (s1i1 type) than vesicles from the SS1 strain (s2i2 VacA), but engineering the SS1 strain to produce s1i1 VacA did not increase the toxin content of its vesicles. Vesicles from all strains tested, including a 60190 isogenic mutant null for VacA, strongly induced interleukin-10 (IL-10) and IL-6 production by human peripheral blood mononuclear cells independently of the infection status of the donor. Finally, we show that H. pylori MV induce T cell apoptosis and that this is enhanced by, but not completely dependent on, the carriage of VacA. Together, these findings suggest a role for H. pylori MV in the stimulation of innate pro- and anti-inflammatory responses and in the suppression of T cell immunity.

Indexed as

ApoptosisBacterial Outer Membrane ProteinsBacterial ProteinsCells, CulturedHelicobacter InfectionsHelicobacter pyloriHost-Pathogen InteractionsHumansJurkat CellsBacterial Outer Membrane ProteinsBacterial ProteinsVacA protein, Helicobacter pylori

Identifiers

PMID24421041
PMCPMC3993389
OpenAlexW2102030338

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.