Evidence map›Paper›PMID 40207800›Full record

ArticleHelicobacter

Chronic Infection With Gastric Helicobacters Induces Hepatic Lesions in Mice.

Lornella Seeneevassen, Elodie Sifré, Sadia Khalid, Mathilde Managau, Francis Mégraud, Armelle Ménard, Pierre Dubus, Pirjo Spuul, Christine Varon

Abstract read
In one paragraph

Article in Helicobacter. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Lornella SeeneevassenINSERM U1312, Bordeaux Institute of Oncology, University of Bordeaux, Bordeaux, France.
Elodie SifréINSERM U1312, Bordeaux Institute of Oncology, University of Bordeaux, Bordeaux, France.
Sadia KhalidDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn, Estonia.
Mathilde ManagauINSERM U1312, Bordeaux Institute of Oncology, University of Bordeaux, Bordeaux, France.
Francis MégraudINSERM U1312, Bordeaux Institute of Oncology, University of Bordeaux, Bordeaux, France.
Armelle MénardINSERM U1312, Bordeaux Institute of Oncology, University of Bordeaux, Bordeaux, France.
Pierre DubusINSERM U1312, Bordeaux Institute of Oncology, University of Bordeaux, Bordeaux, France.
Pirjo SpuulDepartment of Chemistry and Biotechnology, Tallinn University of Technology, Tallinn, Estonia.
Christine VaronINSERM U1312, Bordeaux Institute of Oncology, University of Bordeaux, Bordeaux, France.ORCID https://orcid.org/0000-0003-4026-2016

Funding

Conseil Regional d'Aquitaine 20071301017Conseil Regional d'Aquitaine 20081302203Department Biological and Medical Sciences of The University of BordeauxFrench Association Pour la Recherche Contre le Cancer 8412French Institut National du Cancer 07/3D1616/IABC-23-12/NC-NGFrench Ministry of Tertiary Education, Research and Innovation
6 · The paper itself

Abstract

backgroundHelicobacter pylori infection is one of the most prevalent chronic bacterial infections worldwide. This bacillus colonizes the human stomach lifelong, where it induces chronic gastritis, evolving in some cases to gastro-duodenal ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. H. pylori infection has also been associated with extragastric diseases, and clinical data have suggested a role in liver pathogenesis. This retrospective study evaluated the consequences of chronic infection with gastric Helicobacters on liver pathogenesis in a mouse experimental model. MATERIALS AND

methodsC57BL6 mice were infected with either H. felis (n = 12) or five human and mouse-adapted strains of H. pylori (n = 77) for one year. Uninfected mice were used as negative controls (n = 10). Histopathological analysis of paraffin-embedded liver tissue sections was performed, and scores were determined in a double-blind manner for inflammation and steatosis.

resultsMice infected with H. felis and several H. pylori strains developed more liver parenchymal inflammation and steatosis, known precursor lesions of liver carcinogenesis, compared to non-infected mice. The presence of liver lesions was positively correlated with the detection of lesions of the gastric mucosa, more particularly gastric inflammation and metaplasia.

conclusionChronic infection of mice with H. felis and H. pylori induces liver pathogenesis characterized by parenchymal inflammation and steatosis, which may be associated with the severity of gastric histopathological lesions. Understanding H. pylori infection's impact on extragastric lesions could in fine help detect and prevent the emergence of other digestive tract-related diseases.

Indexed as

Helicobacter felisHelicobacter InfectionsHelicobacter pyloriLiverAnimalsChronic DiseaseDisease Models, AnimalFemaleGastric MucosaHumansMaleMiceMice, Inbred C57BLRetrospective Studiesgastric cancerHelicobacter felisHelicobacter pyloriinflammationlivermouse modelsteatosis

Identifiers

PMID40207800
PMCPMC11984071

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.