Evidence map›Paper›PMID 26316793›Full record

ReviewJournal of inflammation research2015

Differential inflammatory response to Helicobacter pylori infection: etiology and clinical outcomes.

Jonathan Richard White, Jody Anne Winter, Karen Robinson

Open access · goldAbstract readReview
In one paragraph

Review in Journal of inflammation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

57 citing papers in PubMed, 105 citations in OpenAlex.

  1. Frequency ofCanadian liver journal · 2026
    Article
  2. Targeting ferroptosis inInternational journal of oncology · 2026
    Review
  3. Review
  4. Article
  5. The Prevalence ofMedicina (Kaunas, Lithuania) · 2025
    Article
  6. Microbiology (Reading, England) · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Frontiers in cellular and infection microbiology · 2025
    Article
  11. Evaluation of theAnti-cancer agents in medicinal chemistry · 2025
    Article
  12. Article
  13. Article
  14. Microorganisms · 2024
    Review
  15. Article
  16. Pivotal role ofFrontiers in medicine · 2024
    Review
  17. Article
  18. Frontiers in cellular and infection microbiology · 2024
    Article
  19. Article
  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

3 authors at 2 institutions in 1 country.

Jonathan Richard WhiteNIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and The University of Nottingham, Nottingham, UK.
Jody Anne WinterInterdisciplinary Biomedical Research Centre, School of Science and Technology, Nottingham Trent University, Nottingham, UK.
Karen RobinsonNIHR Biomedical Research Unit in Gastrointestinal and Liver Diseases at Nottingham University Hospitals NHS Trust and The University of Nottingham, Nottingham, UK.
University of Nottingham · GBNottingham Trent University · GB

Funding

Medical Research Council G0601170
6 · The paper itself

Abstract

The bacterial pathogen Helicobacter pylori commonly colonizes the human gastric mucosa during early childhood and persists throughout life. The organism has evolved multiple mechanisms for evading clearance by the immune system and, despite inducing inflammation in the stomach, the majority of infections are asymptomatic. H. pylori is the leading cause of peptic ulcer disease and gastric cancer. However, disease outcomes are related to the pattern and severity of chronic inflammation in the gastric mucosa, which in turn is influenced by both bacterial and host factors. Despite over 2 decades of intensive research, there remains an incomplete understanding of the circumstances leading to disease development, due to the fascinating complexity of the host-pathogen interactions. There is accumulating data concerning the virulence factors associated with increased risk of disease, and the majority of these have pro-inflammatory activities. Despite this, only a small proportion of those infected with virulent strains develop disease. Several H. pylori virulence factors have multiple effects on different cell types, including the induction of pro- and anti-inflammatory, immune stimulatory, and immune modulatory responses. The expression of multiple virulence factors is also often linked, making it difficult to assess the meaning of their effects in isolation. Overall, H. pylori is thought to usually modulate inflammation and limit acute damage to the mucosa, enabling the bacteria to persist. If this delicate balance is disturbed, disease may then develop.

Indexed as

gastric cancerHelicobacter pyloriinflammationmucosal immunitypeptic ulcer disease

Identifiers

PMID26316793
PMCPMC4540215
OpenAlexW1186144780

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.