ArticleCell death & disease2018
Helicobacter pylori-induced IL-33 modulates mast cell responses, benefits bacterial growth, and contributes to gastritis.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- FOS Knockdown Alleviates Helicobacter pylori-Infected Gastritis by Suppressing Mast Cell Activation and Treg Polarization.Mediators of inflammation · 2026Article
- The Potential Role ofMicroorganisms · 2025Review
- Single-cell RNA sequencing dissects the immunosuppressive signatures in Helicobacter pylori-infected human gastric ecosystem.Nature communications · 2025Article
- Unveiling the Potency of Gardenia Extract AgainstBiomedicines · 2025Article
- Impact of Mast Cell Activation on Neurodegeneration: A Potential Role for Gut-Brain Axis andNeurology international · 2024Review
- The Role ofJournal of clinical medicine · 2024Review
- Tumor-infiltrating mast cells stimulate ICOSJournal of advanced research · 2024Article
- IL-33 Accelerates Chronic Atrophic Gastritis through AMPK-ULK1 Axis Mediated Autolysosomal Degradation of GKN1.International journal of biological sciences · 2024Article
- Impact ofFrontiers in gastroenterology (Lausanne, Switzerland) · 2024Review
- Modulation of innate lymphoid cells by enteric bacterial pathogens.Frontiers in immunology · 2023Review
- Gastric alarmin release: A warning signal in the development of gastric mucosal diseases.Frontiers in immunology · 2022Review
- miR-483-3p Promotes IL-33 Production from Fibroblast-Like Synoviocytes by Regulating ERK Signaling in Rheumatoid Arthritis.Inflammation · 2021Article
- Arrestin domain containing 3 promotes Helicobacter pylori-associated gastritis by regulating protease-activated receptor 1.JCI insight · 2020Article
- IL33 and Mast Cells-The Key Regulators of Immune Responses in Gastrointestinal Cancers?Frontiers in immunology · 2020Review
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Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-induced inflammatory responses are critical for the pathogenesis of Helicobacter pylori (H. pylori)-induced gastritis. IL-33 represents a recently discovered proinflammatory cytokine involved in inflammatory diseases, but its relevance to H. pylori-induced gastritis is unknown. Here, we found that gastric IL-33 mRNA and protein expression were elevated in gastric mucosa of both patients and mice infected with H. pylori, which is positively correlated with bacterial load and the degree of gastritis. IL-33 production was promoted via extracellular regulated protein kinases (ERK) signaling pathway activation by gastric epithelial cells in a cagA-dependent manner during H. pylori infection, and resulted in increased inflammation and bacteria burden within the gastric mucosa. Gastric epithelial cell-derived IL-33 promoted TNF-α production from mast cells in vitro, and IL-33 increased TNF-α production in vivo. Increased TNF-α inhibited gastric epithelial cell proliferation, conducing to the progress of H. pylori-associated gastritis and bacteria colonization. This study defined a patent regulatory networks involving H. pylori, gastric epithelial cell, IL-33, mast cell, and TNF-α, which jointly play a pathological effect within the gastric circumstances. It may be a valuable strategy to restrain this IL-33-dependent pathway in the treatment of H. pylori-associated gastritis.
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