ArticleClinical and experimental immunology2009
Implications for a role of interleukin-23 in the pathogenesis of chronic gastritis and of peptic ulcer disease.
Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- Characterization of cytotoxic Citrobacter braakii isolated from human stomach.FEBS open bio · 2024Article
- Relationship between active Helicobacter pylori infection and risk factors of cardiovascular diseases, a cross-sectional hospital-based study in a Sub-Saharan setting.BMC infectious diseases · 2022Article
- Extracellular vesicles from gastric epithelial GES-1 cells infected withFrontiers in oncology · 2022Article
- The Roles of IL-17, IL-21, and IL-23 in theToxins · 2021Review
- Proinflammatory Cytokine IL-17 Shows a Significant Association withGastroenterology research and practice · 2017Article
- IL-23 Contributes to Control of Chronic Helicobacter Pylori Infection and the Development of T Helper Responses in a Mouse Model.Frontiers in immunology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the role of gastric mucosa for the secretion of interleukin (IL)-23 in chronic gastritis. One hundred and one patients were enrolled; 47 with duodenal ulcer, 33 with gastric ulcer and 31 with chronic gastritis. Biopsies were incubated in the absence/presence of endotoxins. Supernatants were collected and IL-23 and IL-1beta were measured by enzyme-linked immunosorbent assay. Scoring of gastritis was performed according to the updated Sydney score. Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. IL-23 was higher in supernatants of tissue samples of Helicobacter pylori-positive than of H. pylori-negative patients. No differences were recorded in concentrations of IL-23 and IL-1beta between patients with duodenal ulcer, gastric ulcer and chronic gastritis. Positive correlations were found between IL-23 of patients with both duodenal and gastric ulcer and chronic gastritis and the degree of infiltration of neutrophils and monocytes. Similar correlations were observed between IL-23 and IL-1beta. IL-23 secreted by the gastric mucosa could be implicated in the pathogenesis of chronic gastritis. IL-23 was released in the presence of H. pylori from the inflamed gastric mucosa and followed the kinetics of IL-1beta.
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Registered trials
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