{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T20:45:00Z","timestamp":1790369100631,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,3,23]],"date-time":"2026-03-23T00:00:00Z","timestamp":1774224000000},"content-version":"vor","delay-in-days":81,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100016692","name":"Key Research and Development Program of Ningxia","doi-asserted-by":"publisher","award":["2021BEG03037"],"award-info":[{"award-number":["2021BEG03037"]}],"id":[{"id":"10.13039\/100016692","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      (HP) is a major cause of gastritis, yet the epithelial mechanisms linking infection\u2010induced stress to mast cell and Treg responses remain poorly defined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Three datasets (GSE5081, GSE27411, and GSE233973) were integrated and analyzed using weighted gene co\u2010expression network analysis (WGCNA) and machine learning algorithms. Mast cell\u2010related hub gene expressions were evaluated with quantitative real\u2010time polymerase chain reaction (qRT\u2010PCR), and inflammatory cytokines were quantified using the enzyme\u2010linked immunosorbent assay (ELISA). Histopathological changes were evaluated using hematoxylin and eosin (HE), Giemsa, and Warthin\u2010Starry silver staining. Cell apoptosis was assessed by flow cytometry, and mast cell and Treg cell activities were analyzed by Transwell assays, histamine detection, and immunohistochemistry (IHC).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Fos proto\u2010oncogene (FOS), ribonucleotide reductase regulatory subunit M2 (RRM2), and RAD51 recombinase (RAD51) were identified as mast cell\u2010related hub genes, all of which were upregulated in HP\u2010induced gastritis mice. In vitro, HP infection or CagA stimulation increased FOS expression in gastric epithelial cells. FOS knockdown in HP\u2010infected mice alleviated gastric mucosal injury, reduced bacterial burden, and decreased pro\u2010inflammatory cytokine levels. FOS silencing enhanced GES\u20101 cell viability and suppressed apoptosis. In HP\u2010infected GES\u20101 cells, FOS silencing inhibited mast cell migration, cytokine secretion, including C\u2013C motif chemokine ligand 2 (CCL2), interleukin\u201033 (IL\u201033), and stem cell factor (SCF), as well as histamine release, accompanied by reduced Treg polarization and decreased expression of transforming growth factor\u2010\u03b2 and forkhead box P3.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>FOS silencing inhibited mast cell activation and Treg cell polarization in HP\u2010induced gastritis, suggesting its promising value as an intervention point in HP\u2010driven gastritis.<\/jats:p>\n                  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