ArticleCell communication and signaling : CCS2024
Helicobacter pylori disrupts gastric mucosal homeostasis by stimulating macrophages to secrete CCL3.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Helicobacter pylori Infection and Eradication in Relation to Gastroesophageal Reflux Disease.Journal of gastroenterology and hepatology · 2025Pooled it
- Review
- Targeting tumor-associated bacteria in digestive system cancers: carcinogenic mechanisms and nano-regulate platform design.Journal of nanobiotechnology · 2026Review
- Helicobacter pylori infection and liver function alterations in individuals undergoing gastric cancer screening: a cohort study.Scientific reports · 2026Article
- Extracellular Vesicles of Streptococcus anginosus Mediate Gastritis via Epithelial Barrier Disruption and Macrophage-driven Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pathological effects of diabetic mice withWorld journal of diabetes · 2026Article
- Tight junction proteins: Gatekeepers turned facilitators in the pathogenesis of gastric adenocarcinoma.World journal of gastrointestinal oncology · 2026Review
- Research Status and Prospects ofGastroenterology research and practice · 2026Review
- Progress in immunotherapy forFrontiers in cellular and infection microbiology · 2026Review
- Huangjin Shuangshen decoction alleviates chronic atrophic gastritis by suppressing TNF/NF-κB signaling and promoting CFTR-associated gastric mucosal barrier repair.Frontiers in immunology · 2026Article
- Navigating the gastric frontier of mucosal immunity againstFrontiers in immunology · 2026Review
- Coexpression network analysis of gastric adenocarcinoma identifies hub genes as biomarker candidates and their tumor microenvironment associations.Genetics and molecular biology · 2026Article
- Glycolytic reprogramming in precancerous lesions of gastric cancer progression: pathogenesis and therapeutic potential.Frontiers in oncology · 2026Review
- Enhancement of Gastric Mucosal Defense by Phytomedicine in the Context ofBiologics : targets & therapy · 2026Review
- BeyondMedicina (Kaunas, Lithuania) · 2025Review
- Hub genes and common pathogenic mechanisms between COPD and H. pylori infection.Journal, genetic engineering & biotechnology · 2025Article
- Article
- C-FOS promotes the formation of neutrophil extracellular traps and the recruitment of neutrophils in lung metastasis of triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Helicobacter pylori and gastric cancer: mechanisms and new perspectives.Journal of hematology & oncology · 2025Review
- Management of Gastrointestinal Symptoms in Parkinson's Disease.Journal of central nervous system disease · 2025Review
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8 authors.
Funding
Abstract
backgroundHelicobacter pylori (H. pylori) is the predominant etiological agent of gastritis and disrupts the integrity of the gastric mucosal barrier through various pathogenic mechanisms. After H. pylori invades the gastric mucosa, it interacts with immune cells in the lamina propria. Macrophages are central players in the inflammatory response, and H. pylori stimulates them to secrete a variety of inflammatory factors, leading to the chronic damage of the gastric mucosa. Therefore, the study aims to explore the mechanism of gastric mucosal injury caused by inflammatory factors secreted by macrophages, which may provide a new mechanism for the development of H. pylori-related gastritis.
methodsThe expression and secretion of CCL3 from H. pylori infected macrophages were detected by RT-qPCR, Western blot and ELISA. The effect of H. pylori-infected macrophage culture medium and CCL3 on gastric epithelial cells tight junctions were analyzed by Western blot, immunofluorescence and transepithelial electrical resistance. EdU and apoptotic flow cytometry assays were used to detect cell proliferation and apoptosis levels. Dual-luciferase reporter assays and chromatin immunoprecipitation assays were used to study CCL3 transcription factors. Finally, gastric mucosal tissue inflammation and CCL3 expression were analyzed by hematoxylin and eosin staining and immunohistochemistry.
resultsAfter H. pylori infection, CCL3 expressed and secreted from macrophages were increased. H. pylori-infected macrophage culture medium and CCL3 disrupted gastric epithelial cells tight junctions, while CCL3 neutralizing antibody and receptor inhibitor of CCL3 improved the disruption of tight junctions between cells. In addition, H. pylori-infected macrophage culture medium and CCL3 recombinant proteins stimulated P38 phosphorylation, and P38 phosphorylation inhibitor improved the disruption of tight junctions between cells. Besides, it was identified that STAT1 was a transcription factor of CCL3 and H. pylori stimulated macrophage to secret CCL3 through the JAK1-STAT1 pathway. Finally, after mice were injected with murine CCL3 recombinant protein, the gastric mucosal injury and inflammation were aggravated, and the phosphorylation level of P38 was increased.
conclusionsIn summary, our findings demonstrate that H. pylori infection stimulates macrophages to secrete CCL3 via the JAK1-STAT1 pathway. Subsequently, CCL3 damages gastric epithelial tight junctions through the phosphorylation of P38. This may be a novel mechanism of gastric mucosal injury in H. pylori-associated gastritis.
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