ArticleGastroenterology2019
Tropism for Spasmolytic Polypeptide-Expressing Metaplasia Allows Helicobacter pylori to Expand Its Intragastric Niche.
Article in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 77 citations in OpenAlex.
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- Regulation of STK38 by autophagy governs YAP1 activity during paligenosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026Review
- Paligenosis: dual potential of mature cell plasticity in regeneration and tumorigenesis.MedScience · 2026Review
- Pathogenicity and virulence ofVirulence · 2025Review
- Gastric organoids: A promising model for studying "inflammation-cancer" transition in atrophic gastritis.World journal of clinical oncology · 2025Review
- Revolutionizing Gastric Cancer Prevention: Novel Insights on Gastric Mucosal Inflammation-Cancer Transformation and Chinese Medicine.Chinese journal of integrative medicine · 2025Review
- Patterns of sialyl-Lewis X expression predict gastric histopathology.Diagnostic pathology · 2025Article
- Repeat Ascaris challenge reduces worm intensity through gastric cellular reprograming.PLoS neglected tropical diseases · 2025Article
- Cellular lineage origins of spasmolytic polypeptide-expressing metaplasia (SPEM): persistent and intensifying debates.Frontiers in oncology · 2025Review
- Advances in modeling gastric intestinal metaplasia: a comprehensive review of experimental models and mechanistic insights.Frontiers in oncology · 2025Review
- H. Pylori-Facilitated TERT/Wnt/β-Catenin Triggers Spasmolytic Polypeptide-Expressing Metaplasia and Oxyntic Atrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Emerging role of spasmolytic polypeptide-expressing metaplasia in gastric cancer.Journal of gastrointestinal oncology · 2024Review
- Molecular insights into the fine-tuning of pH-dependent ArsR-mediated regulation of the SabA adhesin in Helicobacter pylori.Nucleic acids research · 2024Article
- Comparison of gastric inflammation and metaplasia induced byMicrobiology spectrum · 2024Article
- Review
- RNF115 aggravates tumor progression through regulation of CDK10 degradation in thyroid carcinoma.Cell biology and toxicology · 2024Article
- Host gastric corpus microenvironment facilitates Ascaris suum larval hatching and infection in a murine model.PLoS neglected tropical diseases · 2024Article
- ASCC3 promotes the immunosuppression and progression of non-small cell lung cancer by impairing the type I interferon response via CAND1-mediated ubiquitination inhibition of STAT3.Journal for immunotherapy of cancer · 2023Article
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsIn patients with chronic Helicobacter pylori (H pylori) infection, parietal and chief cell atrophy in the gastric corpus, a process known as spasmolytic polypeptide-expressing metaplasia (SPEM), increases the risk for progression to cancer. The relation between H pylori and these metaplastic changes is unclear. We investigated whether H pylori localizes to regions of SPEM.
methodsWe developed an in situ adherence assay in which we incubated H pylori with free-floating tissue sections from the gastric corpora of mice; we assessed H pylori distribution along the gastric unit by immunofluorescence. We analyzed the interactions of H pylori with tissue collected from mice with acute SPEM, induced by high-dose tamoxifen. We also evaluated how adhesin-deficient H pylori strains, chemical competition assays, and epithelial glycosylation affected H pylori adhesion to SPEM glands. Mice colonized with the mouse-adapted PMSS1 strain were analyzed for H pylori colonization in vivo during tamoxifen-induced SPEM or after decrease of stomach acid with omeprazole.
resultsCompared with uninjured glands, H pylori penetrated deep within SPEM glands, in situ, through interaction of its adhesin, SabA, with sialyl-Lewis X, which expanded in SPEM. H pylori markedly increased gastric corpus colonization when SPEM was induced, but this proximal spread reversed in mice allowed to recover from SPEM. Decreasing corpus acidity also promoted proximal spread. However, H pylori penetrated deep within corpus glands in vivo only when sialyl-Lewis X expanded during SPEM.
conclusionsHelicobacter pylori differentially binds SPEM glands in situ and in mice, in large part by interacting with sialyl-Lewis X. Our findings indicate that H pylori expands its niche into the gastric corpus by promoting and exploiting epithelial metaplastic changes that can lead to tumorigenesis.
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