ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Microorganisms in Vertebrate Digestive Systems
Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1565392
This article is part of the Research TopicThe Gut Microbiome's Role in Gastric Cancer: Mechanisms and TherapiesView all 12 articles
Gastric mucosal proteomic analysis reveals the role of TGF-β signaling pathway in gastritis associated with Helicobacter pylori infection
Provisionally accepted
- 1Guizhou Medical University, Guiyang, Guizhou Province, China
- 2Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province, China
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Helicobacter pylori (H. pylori) infection induces chronic infla mmation of the gastric mucosa. There is a close relationship between Th1 7/Treg cell imbalance and adverse outcomes associated with H. pylori inf ection. The differentiation and development of both Th17 and Treg cells r equire the regulatory involvement of TGF-β. However, the regulatory role of the TGF-β signaling pathway in H. pylori-induced gastritis remains un clear. The aim of this study was to investigate the impact of H. pylori infe ction on the expression of TGF-β pathway proteins in patients with chroni c gastritis, as well as changes in Th17 and Treg cells and their cytokine ex pression levels. In this study, gastric mucosal proteomic analysis revealed that differentially expressed proteins were enriched in signaling pathway s such as TGF-β, MAPK, and Th17. Experiments demonstrated that TGF-β1 and TAK1 mRNA levels, along with their protein expression, were inc reased in both the peripheral blood and gastric mucosa of H. pylori-infect ed gastritis patients. Compared to the negative control group, H. pylori-in fected gastritis patients showed elevated levels of Th17 and Treg cell tran scription factors (RORγt and Foxp3 mRNA) in peripheral blood and gastri c mucosa, as well as increased IL-17 and Foxp3 protein expression in gas tric mucosa and elevated IL-17 and IL-10 levels in peripheral blood. Ani mal experiments revealed a decreased Th17/Treg ratio in H. pylori-infecte d gastritis mice. We hypothesize that H. pylori infection may participate i n gastric mucosal inflammatory responses by activating the TGF-β signali ng pathway and interacting with the immune balance between Th17 and T reg cells during inflammation. These findings provide new strategies for t he prevention and treatment of H. pylori-induced gastritis. This translatio n maintains medical accuracy while ensuring fluency and adherence to sta ndard scientific writing conventions. Let me know if you'd like any refine ments!
Keywords: Helicobacter pylori-induced gastritis, Proteomics, Transfor ming growth factor beta 1, Transforming growth factor-β-activated kinase, T helper cell 17; Regulatory T cells
Received: 23 Jan 2025; Accepted: 25 Aug 2025.
Copyright: © 2025 Zhu, Xiong, He, Sun and Mo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Fei Mo, Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, Guizhou Province, China
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