Authors
Jian Chen, Li Zhou, Ling Li, Yue Wang
Published in
Archives of microbiology. Volume 208. Issue 11. Aug 11, 2026. Epub Aug 11, 2026.
Abstract
Helicobacter pylori (H. pylori) is a major cause of chronic gastritis and gastric cancer. Macrophages are key regulators of gastric immunity, yet the mechanisms by which H. pylori reprogram macrophage activation and suppresses host immune responses remain unclear. RAW264.7 macrophages were infected with H. pylori PMSS1. Macrophage polarization, cytokine secretion, and JAK3/STAT5-SOCS3 signaling were examined by qRT-PCR, Western blotting, flow cytometry, and ELISA. Ritlecitinib was used to inhibit JAK3. Primary naive CD4⁺ T cells were treated with macrophage-conditioned medium to assess proliferation, CD25/CD69 activation, and FoxP3⁺ Treg differentiation. SOCS3 knockdown was used to evaluate rescue effects. H. pylori significantly promoted M1 macrophage polarization, with increased CD86, iNOS, MHC II, TNF-α, and IFN-γ and decreased CD163, Arg1, TGF-β, and IL-10 (p < 0.05). H. pylori also upregulated JAK3, STAT5, and SOCS3, while Ritlecitinib attenuated inflammatory gene expression (p < 0.05). Hp-CM significantly inhibited primary CD4⁺ T-cell proliferation, CD25/CD69 activation, and CD4⁺CD25⁺FoxP3⁺ Treg differentiation (p < 0.05). SOCS3 knockdown partially restored these CD4⁺ T-cell responses (p < 0.05). H. pylori promotes M1 macrophage polarization and impairs CD4⁺ T-cell immunity through JAK3/STAT5-SOCS3-mediated immune dysregulation. This mechanism contributes to chronic immune dysregulation and supports bacterial persistence, identifying JAK3/SOCS3 as potential therapeutic targets.
PMID:
42579134
Bibliographic data and abstract were imported from PubMed on 11 Aug 2026.
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