ArticleFrontiers in immunology2016
Helicobacter pylori Activates HMGB1 Expression and Recruits RAGE into Lipid Rafts to Promote Inflammation in Gastric Epithelial Cells.
Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- KaiWei JianPI Ointment Downregulates Fcgbp and Modulates HMGB1/TLR4 Signaling to Combat Ferroptosis inThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2026Article
- Electroacupuncture enhances nerve regeneration and functional recovery in a rat model of median nerve transection.IBRO neuroscience reports · 2025Article
- Article
- Advanced glycation end products in gastric cancer: A promising future.World journal of clinical oncology · 2024Article
- Therapeutic potential of Phycocyanin in gastrointestinal cancers and related disorders.Molecular biology reports · 2024Review
- The interaction between autophagy, Helicobacter pylori, and gut microbiota in gastric carcinogenesis.Trends in microbiology · 2023Review
- Article
- Glycyrrhizin, an inhibitor of HMGB1 induces autolysosomal degradation function and inhibits Helicobacter pylori infection.Molecular medicine (Cambridge, Mass.) · 2023Article
- Toll-like Receptor 9 Pathway Mediates SchlafenGastroenterology · 2022Article
- Role of lipid rafts in persistentAnnals of translational medicine · 2022Review
- Gastric alarmin release: A warning signal in the development of gastric mucosal diseases.Frontiers in immunology · 2022Review
- Magic Peptide: Unique Properties of the LRR11 Peptide in the Activation of Leukotriene Synthesis in Human Neutrophils.International journal of molecular sciences · 2021Article
- The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- CoQJournal of clinical medicine · 2020Article
- Article
- Article
- ProbioticJournal of clinical medicine · 2019Article
- Article
- Coalescence of RAGE in Lipid Rafts in Response to Cytolethal Distending Toxin-Induced Inflammation.Frontiers in immunology · 2019Article
- Contribution of myo-inositol oxygenase in AGE:RAGE-mediated renal tubulointerstitial injury in the context of diabetic nephropathy.American journal of physiology. Renal physiology · 2018Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori infection is associated with several gastrointestinal disorders in the human population worldwide. High-mobility group box 1 (HMGB1), a ubiquitous nuclear protein, mediates various inflammation functions. The interaction between HMGB1 and receptor for advanced glycation end-products (RAGE) triggers nuclear factor (NF)-κB expression, which in turn stimulates the release of proinflammatory cytokines, such as interleukin (IL)-8, and enhances the inflammatory response. However, how H. pylori activates HMGB1 expression and mobilizes RAGE into cholesterol-rich microdomains in gastric epithelial cells to promote inflammation has not been explored. In this study, we found that HMGB1 and RAGE expression increased significantly in H. pylori-infected cells compared with -uninfected cells. Blocking HMGB1 by neutralizing antibody abrogated H. pylori-elicited RAGE, suggesting that RAGE expression follows HMGB1 production, and silenced RAGE-attenuated H. pylori-mediated NF-κB activation and IL-8 production. Furthermore, significantly more RAGE was present in detergent-resistant membranes extracted from H. pylori-infected cells than in those from -uninfected cells, indicating that H. pylori exploited cholesterol to induce the HMGB1 signaling pathway. These results indicate that HMGB1 plays a crucial role in H. pylori-induced inflammation in gastric epithelial cells, which may be valuable in developing treatments for H. pylori-associated diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.