ArticleBMC gastroenterology2017
Helicobacter-induced gastric inflammation alters the properties of gastric tissue stem/progenitor cells.
Article in BMC gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Nanomechanical Hallmarks ofInternational journal of molecular sciences · 2021Trial
- Pristimerin ameliorates spasmolytic polypeptide-expressing metaplasia by modulatingWorld journal of gastroenterology · 2026Article
- Advances in modeling gastric intestinal metaplasia: a comprehensive review of experimental models and mechanistic insights.Frontiers in oncology · 2025Review
- Impact of bacteroides uniformis on fatty liver hemorrhagic syndrome in dawu golden phoenix laying hens: modulation of gut microbiota and arachidonic acid metabolism.Frontiers in microbiology · 2025Article
- Impact of enteric bacterial infections at and beyond the epithelial barrier.Nature reviews. Microbiology · 2023Review
- Role of spasmolytic polypeptide-expressing metaplasia in gastric mucosal diseases.American journal of cancer research · 2023Review
- Jian-Pi-Yi-Qi-Fang ameliorates chronic atrophic gastritis in rats through promoting the proliferation and differentiation of gastric stem cells.Annals of translational medicine · 2022Article
- 3D Human Organoids: The Next "Viral" Model for the Molecular Basis of Infectious Diseases.Biomedicines · 2022Review
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- Curcumin Oxidation Is Required for Inhibition ofFrontiers in cellular and infection microbiology · 2021Article
- Organoid Models of Tumor Immunology.Trends in immunology · 2020Review
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- Guilt by association: intestinal metaplasia does not progress to gastric cancer.Current opinion in gastroenterology · 2018Review
- Autoimmunity and Gastric Cancer.International journal of molecular sciences · 2018Review
- Correction to: Helicobacter-induced gastric inflammation alters the properties of gastric tissue stem/progenitor cells.BMC gastroenterology · 2018Article
- Activation of Signal Transduction and Activator of Transcription 3 Signaling Contributes toGastroenterology research and practice · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlthough Helicobacter-induced gastric inflammation is the major predisposing factor for gastric carcinogenesis, the precise mechanism by which chronic gastritis causes gastric cancer remains unclear. Intestinal and spasmolytic polypeptide-expressing metaplasia (SPEM) is considered as precancerous lesions, changes in epithelial tissue stem/progenitor cells after chronic inflammation has not been clarified yet. In this study, we utilized three-dimensional gastric epithelial cell culture systems that could form organoids, mimicking gastric epithelial layer, and characterized the changes in epithelial cells after chronic Helicobacter felis infection.
methodsWe used three mice model; 1) long-term H. felis infection, 2) H. felis eradication, and 3) MNU chemical carcinogenesis model. We performed cRNA microarray analysis after organoid culture, and analyzed the effects of chronic gastric inflammation on tissue stem cells, by the size of organoid, mRNA expression profile and immunohistochemical analysis.
resultsThe number of organoids cultured from gastric epithelial cells was significantly higher in organoids isolated from H. felis-infected mice compared with those from uninfected gastric mucosa. Based on the mRNA expression profile, we found that possible stem cell markers such as Cd44, Dclk1, and genes associated with the intestinal phenotype, such as Villin, were increased in organoids isolated from H. felis-infected mucosa compared with the control. The upregulation of these genes were cancelled after H. felis eradication. In a xenograft model, tumors were generated only from organoids cultured from carcinogen-treated gastric mucosa, not from H. felis infected mucosa or control organoids.
conclusionsOur results suggested that, as a possible mechanism of gastric carcinogenesis, chronic inflammation induced by H. felis infection increased the number of tissue stem/progenitor cells and the expression of stem cell markers. These findings suggest that chronic inflammation may alter the direction of differentiation toward undifferentiated state and that drawbacks may enable cells to redifferentiate to intestinal metaplasia or neoplasia.
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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.