Evidence map›Paper›PMID 40011208›Full record

ArticleHelicobacter

The Gastric Microbiota Invade the Lamina Propria in Helicobacter pylori-Associated Gastritis and Precancer.

Harriet J Giddings, Ana Teodósio, Jordanne Jones, Jack L McMurray, Kelly Hunter, Riad Alame, Isaac Gardiner, Zainab Abdawn, William Butterworth, Ian R Henderson and 3 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Helicobacter. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Clinical significance of a possible route of transmission ofWorld journal of gastrointestinal pathophysiology · 2026
    Article
  4. Article
  5. Review
  6. Laser capture microdissection.Nature reviews. Methods primers · 2025
    Article
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

13 authors.

Harriet J GiddingsInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Ana TeodósioBirmingham Tissue Analytics, University of Birmingham, Birmingham, UK.
Jordanne JonesBirmingham Tissue Analytics, University of Birmingham, Birmingham, UK.
Jack L McMurrayBirmingham Tissue Analytics, University of Birmingham, Birmingham, UK.
Kelly HunterBirmingham Tissue Analytics, University of Birmingham, Birmingham, UK.
Riad AlameQueen Elizabeth Hospital, University Hospital Birmingham NHS Foundation Trust, Birmingham, UK.
Isaac GardinerInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Zainab AbdawnQueen Elizabeth Hospital, University Hospital Birmingham NHS Foundation Trust, Birmingham, UK.
William ButterworthDepartment of Immunology and Immunotherapy, School of Infection, Inflammation and Immunology, College of Medicine and Health, University of Birmingham, Birmingham, UK.
Ian R HendersonInstitute for Molecular Biosciences, University of Queensland, Brisbane, Australia.
Jeffrey A ColeInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Claire D Shannon-LoweDepartment of Immunology and Immunotherapy, School of Infection, Inflammation and Immunology, College of Medicine and Health, University of Birmingham, Birmingham, UK.
Amanda E Rossiter-PearsonInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.ORCID https://orcid.org/0000-0002-8567-7998

Funding

Cancer Research UK EDDPMA-Nov21\100008Royal Society RGS\R2\192312
6 · The paper itself

Abstract

backgroundStomach cancer is the fourth leading cause of cancer-related deaths worldwide. Helicobacter pylori is the main risk factor for gastric adenocarcinoma (GAC), yet the precise mechanism underpinning this association remains controversial. Gastric intestinal metaplasia (GIM) represents the precancerous stage and follows H. pylori-associated chronic gastritis (CG). Sequencing studies have revealed fewer H. pylori and more non-H. pylori bacteria in GAC. However, the spatial organization of the gastric microbiota in health and disease is unknown. MATERIALS AND

methodsHere, we have combined RNA in situ hybridization and immunohistochemistry to detect H. pylori, non-H. pylori bacteria, and host cell markers (E-cadherin, Mucins 5AC and 2) on tissue sections from patients with CG (n = 15) and GIM (n = 17).

resultsQuantitative analysis of whole slide scans revealed significant correlations of H. pylori and other bacteria in CG and GIM. In contrast to sequencing studies, significantly fewer non-H. pylori bacteria were detected in H. pylori-negative patients. Importantly, whilst H. pylori exclusively colonized the gastric glands, non-H. pylori bacteria invaded the lamina propria in 6/9 CG and 8/10 GIM H. pylori-positive patients. A rapid and cost-effective modified Gram stain was used to confirm these findings and enabled detection of non-H. pylori bacteria in GIM samples.

conclusionsThe invasion of the gastric lamina propria by non-H. pylori bacteria during H. pylori-associated CG and GIM represents an overlooked phenomenon in cancer progression. Further work must determine the mechanisms underlying the synergistic roles of H. pylori and other bacteria in carcinogenesis. This observation should redirect attempts to prevent, diagnose, and treat GAC.

Indexed as

Gastric MucosaGastritisGastrointestinal MicrobiomeHelicobacter InfectionsHelicobacter pyloriPrecancerous ConditionsAdultAgedFemaleHumansImmunohistochemistryIn Situ HybridizationMaleMetaplasiaMiddle AgedStomach Neoplasmsgastric adenocarcinomaHelicobacter pylorimicrobiomespatial biology

Identifiers

PMID40011208
PMCPMC11865006

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Registered trials

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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.