ArticleCellular and molecular gastroenterology and hepatology2018
Interleukin-17A Promotes Parietal Cell Atrophy by Inducing Apoptosis.
Article in Cellular and molecular gastroenterology and hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 62 citations in OpenAlex.
- The origins and progression of pyloric metaplasia following gastric mucosal injury.Physiological reviews · 2026Review
- Autoimmune gastritis: emerging insights and clinical management.Nature reviews. Gastroenterology & hepatology · 2026Review
- Gastric Microbiota Dysbiosis and Microbiome-Based Interventions in Chronic Atrophic Gastritis.Nutrients · 2026Review
- Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026Review
- Immunological mechanisms of autoimmune gastritis.Clinical and experimental medicine · 2026Review
- Roles of interleukins in spasmolytic polypeptide‑expressing metaplasia (Review).International journal of oncology · 2026Review
- Inflammatory Cytokines as Potential Inducements of Early Gastric Mucosal Lesions inGastroenterology research and practice · 2026Article
- CXCR4 inhibition alleviates prostatic inflammation and pelvic pain via suppressing Th17 cell differentiation and oxidative stress in EAP mice.International journal of biological sciences · 2026Article
- Exploring the frontier of oral nanomedicine in colorectal cancer therapy: Folate-targeted 5FU-Nisin-Selenium conjugates and probiotic-rich diets as a novel approach.Asian journal of pharmaceutical sciences · 2025Article
- Amikacin toxicity revisited: pentoxifylline offers protection in high-risk treatment scenarios.AMB Express · 2025Article
- Impact of Curcumin on the IL-17A-Mediated p53-Fibrinolytic System: Mouse Proteomics and Integrated Human Fibrosis scRNAseq Insights.Inflammation · 2025Article
- The Role of Cancer Organoids in Ferroptosis, Pyroptosis, and Necroptosis: Functions and Clinical Implications.Biomolecules · 2025Review
- H. Pylori-Facilitated TERT/Wnt/β-Catenin Triggers Spasmolytic Polypeptide-Expressing Metaplasia and Oxyntic Atrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanism of Chronic Atrophic Gastritis: A 20-Year Bibliometric Analyses.Journal of inflammation research · 2025Article
- A Natural Peptide from A Traditional Chinese Medicine Has the Potential to Treat Chronic Atrophic Gastritis by Activating Gastric Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role and research progress of spasmolytic polypeptide‑expressing metaplasia in gastric cancer (Review).International journal of oncology · 2024Article
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- IL-33 Accelerates Chronic Atrophic Gastritis through AMPK-ULK1 Axis Mediated Autolysosomal Degradation of GKN1.International journal of biological sciences · 2024Article
- Pro- and anti-inflammatory cytokines: the hidden keys to autoimmune gastritis therapy.Frontiers in pharmacology · 2024Review
- Histopathological features of glandular atrophy of the lamina propria of the gastric mucosa during its occurrence and development.BMC gastroenterology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsAtrophic gastritis caused by chronic inflammation in the gastric mucosa leads to the loss of gastric glandular cells, including acid-secreting parietal cells. Parietal cell atrophy in a setting of chronic inflammation induces spasmolytic polypeptide expressing metaplasia, a critical step in gastric carcinogenesis. However, the mechanisms by which inflammation causes parietal cell atrophy and spasmolytic polypeptide expressing metaplasia are not well defined. We investigated the role of interleukin-17A (IL-17A) in causing parietal cell atrophy.
methodsA mouse model of autoimmune atrophic gastritis was used to examine IL-17A production during early and late stages of disease. Organoids derived from corpus glands were used to determine the direct effects of IL-17A on gastric epithelial cells. Immunofluorescent staining was used to examine IL-17A receptors and the direct effect of signaling on parietal cells. Mice were infected with an IL-17A-producing adenovirus to determine the effects of IL-17A on parietal cells in vivo. Finally, IL-17A neutralizing antibodies were administered to mice with active atrophic gastritis to evaluate the effects on parietal cell atrophy and metaplasia.
resultsIncreased IL-17A correlated with disease severity in mice with chronic atrophic gastritis. IL-17A caused caspase-dependent gastric organoid degeneration, which could not be rescued with a necroptosis inhibitor. Parietal cells expressed IL-17A receptors and IL-17A treatment induced apoptosis in parietal cells. Overexpressing IL-17A in vivo induced caspase-3 activation and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling staining in parietal cells. Finally, IL-17A neutralizing antibody decreased parietal cell atrophy and metaplasia in mice with chronic atrophic gastritis.
conclusionsThese data identify IL-17A as a cytokine that promotes parietal cell apoptosis during atrophic gastritis, a precursor lesion for gastric cancer.
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Registered trials
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.