ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2024
Sustained exposure to Helicobacter pylori induces immune tolerance by desensitizing TLR6.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Beyond Infection: Mitochondrial Reprogramming and Immunometabolic Adaptation inDiseases (Basel, Switzerland) · 2026Article
- Helicobacter pylori infection is causally associated with extra-gastric tumors: a Mendelian randomization study.Discover oncology · 2026Article
- Progress in immunotherapy forFrontiers in cellular and infection microbiology · 2026Review
- Glucolipid Metabolic Disorders andInternational journal of endocrinology · 2026Review
- Mechanisms and therapeutic strategies for immunotherapy resistance in gastric cancer.Cancer cell international · 2025Review
- Identification and experimental validation of biomarkers associated with macrophages in myocardial ischemia-reperfusion injury.Scientific reports · 2025Article
- An pH-responsive liposome for the targeted treatment ofMaterials today. Bio · 2025Article
- Biphasic Adaptations of Gastric Epithelial Cells in ChronicInternational journal of molecular sciences · 2025Article
- An AI-Designed Antibody-Engineered Probiotic Therapy Targeting Urease to CombatMicroorganisms · 2025Article
- Risk factors and clinical prediction models for short-term recurrence after endoscopic surgery in patients with colorectal polyps.World journal of gastrointestinal surgery · 2025Article
- The Gut Microbiome's Impact on the Pathogenesis and Treatment of Gastric Cancer-An Updated Literature Review.Cancers · 2025Review
- Toll-Like Receptors in the Immunotherapy Era: Dual-Edged Swords of Tumor Immunity and Clinical Translation.MedComm · 2025Review
- Review
- Research advances of the establishment and characterization ofFrontiers in microbiology · 2025Review
- A New Medical Evaluation for Gastric Cancer Patients to Increase the Success Rate of Immunotherapy: A 2024 Update.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Trained Immunity and Trained Tolerance: The Case ofInternational journal of molecular sciences · 2024Review
- Review
- Current study of pathogenetic mechanisms and therapeutics of chronic atrophic gastritis: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Novel therapeutic regimens againstFrontiers in microbiology · 2024Review
- Progranulin inhibits autophagy to facilitate intracellular colonization ofFrontiers in cellular and infection microbiology · 2024Article
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori (H. pylori, Hp) has been designated a class I carcinogen and is closely associated with severe gastric diseases. During colonization in the gastric mucosa, H. pylori develops immune escape by inducing host immune tolerance. The gastric epithelium acts as the first line of defense against H. pylori, with Toll-like receptors (TLRs) in gastric epithelial cells being sensitive to H. pylori components and subsequently activating the innate immune system. However, the mechanism of immune tolerance induced by H. pylori through the TLR signalling pathway has not been fully elucidated. In this research, we detected the expression of TLRs and inflammatory cytokines in GES-1 cells upon sustained exposure to H. pylori or H. pylori lysate from 1 to 30 generations and in Mongolian gerbils infected with H. pylori for 5 to 90 weeks. We found that the levels of TLR6 and inflammatory cytokines first increased and then dropped during the course of H. pylori treatment in vitro and in vivo. The restoration of TLR6 potentiated the expression of IL-1β and IL-8 in GES-1 cells, which recruited neutrophils and reduced the colonization of H. pylori in the gastric mucosa of gerbils. Mechanistically, we found that persistent infection with H. pylori reduces the sensitivity of TLR6 to bacterial components and regulates the expression of inflammatory cytokines in GES-1 cells through TLR6/JNK signaling. The TLR6 agonist obviously alleviated inflammation in vitro and in vivo. Promising results suggest that TLR6 may be a potential candidate immunotherapy drug for H. pylori infection.
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