ArticleMediators of inflammation2026
FOS Knockdown Alleviates Helicobacter pylori-Infected Gastritis by Suppressing Mast Cell Activation and Treg Polarization.
Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Targeting regulatory T cell plasticity in gastric cancer: a unified bimodal model and precision immunotherapy paradigm: a hypothesis-generating review.Frontiers in oncology · 2026Article
- FOS Knockdown Alleviates Helicobacter pylori-Infected Gastritis by Suppressing Mast Cell Activation and Treg Polarization.Mediators of inflammation · 2026Article
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Abstract
backgroundHelicobacter pylori (HP) is a major cause of gastritis, yet the epithelial mechanisms linking infection-induced stress to mast cell and Treg responses remain poorly defined.
methodsThree datasets (GSE5081, GSE27411, and GSE233973) were integrated and analyzed using weighted gene co-expression network analysis (WGCNA) and machine learning algorithms. Mast cell-related hub gene expressions were evaluated with quantitative real-time polymerase chain reaction (qRT-PCR), and inflammatory cytokines were quantified using the enzyme-linked immunosorbent assay (ELISA). Histopathological changes were evaluated using hematoxylin and eosin (HE), Giemsa, and Warthin-Starry 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).
resultsFos proto-oncogene (FOS), ribonucleotide reductase regulatory subunit M2 (RRM2), and RAD51 recombinase (RAD51) were identified as mast cell-related hub genes, all of which were upregulated in HP-induced gastritis mice. In vitro, HP infection or CagA stimulation increased FOS expression in gastric epithelial cells. FOS knockdown in HP-infected mice alleviated gastric mucosal injury, reduced bacterial burden, and decreased pro-inflammatory cytokine levels. FOS silencing enhanced GES-1 cell viability and suppressed apoptosis. In HP-infected GES-1 cells, FOS silencing inhibited mast cell migration, cytokine secretion, including C-C motif chemokine ligand 2 (CCL2), interleukin-33 (IL-33), and stem cell factor (SCF), as well as histamine release, accompanied by reduced Treg polarization and decreased expression of transforming growth factor-β and forkhead box P3.
conclusionFOS silencing inhibited mast cell activation and Treg cell polarization in HP-induced gastritis, suggesting its promising value as an intervention point in HP-driven gastritis.
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