ArticleClinical and experimental immunology2025
Dynamic changes of host immune response during Helicobacter pylori-induced gastric cancer development.
Article in Clinical and experimental immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Advances inOncology letters · 2026Review
- Chronic psychological stress and gastric cancer: bidirectional associations, biological mechanisms, and clinical implications-a narrative review.Journal of gastrointestinal oncology · 2026Review
- The Oral-Gastric Microbial Axis in Gastric Cancer: Mechanisms Underlying Development and Progression.Cancers · 2026Review
- Integrated bioinformatic and machine learning analysis identifies MCM7 and ADAM17 as potential biomarkers for early stage gastric cancer.Journal of gastrointestinal oncology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
introductionHelicobacter pylori infection is the main risk factor for gastric cancer (GC). Chronic inflammation is usually induced by H. pylori infection and is accompanied by inherent immune disorders. However, the dynamic changes in the host immune response associated with the transition from normal to metaplasia, dysplasia, and GC are largely undefined.
methodWe established the H. pylori-induced GC mice model. The gastric mucosa of H. pylori-infected mice was subjected to RNA-sequencing analysis at different stages. We analyzed systemic immune disturbances in the spleen and changes in serum inflammatory cytokines during GC development, including gastritis, premalignant lesions (pre-GC), and GC stages.
resultsRNA-sequencing analysis of the gastric mucosa of H. pylori-infected mice highlighted the important role of immune-associated pathways (especially inflammatory pathways) during GC development. Immune cell proportion analysis revealed the stage-dependent involvement of key immune cell types, including increased Th17 cells in early gastritis and pre-GC stages and decreased central memory CD4+ and CD8+ T cells during GC transition. Serum inflammatory cytokine analysis showed that IL-6 and IL-10 levels significantly increased, whereas IL-23 levels decreased during the GC stage.
conclusionIn summary, we illustrated systemic immune disturbances in the spleen and changes in serum inflammatory cytokines during GC development. Th17 cells were involved in early gastritis and premalignant processes, while central memory T cells participated in GC transition. Our findings provide valuable insights into identifying key inflection points and associated biomarkers for the early detection, diagnosis, and treatment of GC.
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