{"@type": "dcat:Dataset", "accessLevel": "public", "bureauCode": ["009:25"], "contactPoint": {"@type": "vcard:Contact", "fn": "NIH", "hasEmail": "mailto:info@nih.gov"}, "description": "Background\n          Helicobacter pylori is the main risk factor for the development of non-cardia gastric cancer. Increased proliferation of the gastric mucosa is a feature of H. pylori infection. Mucosal interkeukin-1\u03b2 production is increased in H. pylori infection and IL-1\u03b2 genotypes associated with increased pro-inflammatory activity are risk factors for the development of gastric cancer. The effect of IL-1\u03b2 on gastric epithelial cell proliferation has been examined in this study.\n        \n        \n          Methods\n          AGS cells were cultured with IL-1\u03b2. DNA synthesis was assed by [3H]thymidine incorporation and total viable cell numbers by MTT assay.\n        \n        \n          Results\n          IL-1\u03b2 dose dependently increased DNA synthesis and cell numbers. The enhanced proliferation was blocked by interleukin-1 receptor antagonist. Addition of neutralising antibody to GM-CSF reduced IL-1\u03b2-stimulated proliferation by 31 \u00b1 4 %. GM-CSF alone significantly stimulated proliferation. Addition or neutralisation of IL-8 had no effect on basal or IL-1\u03b2-stimulated proliferation. The tyrosine kinase inhibitor genistein completely blocked IL-1\u03b2-stimulated proliferation and inhibition of the extracellular signal related kinase pathway with PD 98059 inhibited IL-1\u03b2 stimulated proliferation by 58 \u00b1 5 %.\n        \n        \n          Conclusions\n          IL-1\u03b2 stimulates proliferation in gastric epithelial cells. Autocrine stimulation by GM-CSF contributes to this proliferative response. Signalling via tyrosine kinase activity is essential to the mitogenic response to IL-1\u03b2. The extracellular signal related kinase pathway is involved in, but not essential to downstream signalling. IL-1\u03b2 may contribute to the hyperproliferation seen in H. pylori- infected gastric mucosa, and be involved in the carcinogenic process.", "distribution": [{"@type": "dcat:Distribution", "description": "Visit the original government dataset for complete information, documentation, and data access.", "downloadURL": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC103665/", "mediaType": "text/html", "title": "Official Government Data Source"}], "identifier": "https://healthdata.gov/api/views/p5ff-6dqr", "issued": "2025-07-14", "keyword": ["cell-proliferation", "gastric-cancer", "interleukin-1", "interleukin-1\u03b2", "nih"], "landingPage": "https://healthdata.gov/d/p5ff-6dqr", "modified": "2025-09-06", "programCode": ["009:033"], "publisher": {"@type": "org:Organization", "name": "National Institutes of Health"}, "theme": ["NIH"], "title": "Effect of Interlukin-1\u03b2 on proliferation of gastric epithelial cells in culture"}