Mediators of inflammation · 2026
FOS Knockdown Alleviates Helicobacter pylori-Infected Gastritis by Suppressing Mast Cell Activation and Treg Polarization.
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Ma Wen, Han Ruidong, Wang Lei
Аннотация
BACKGROUND: Helicobacter 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.
METHODS: Three 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).
RESULTS: Fos 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.
CONCLUSION: FOS 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.
METHODS: Three 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).
RESULTS: Fos 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.
CONCLUSION: FOS 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.