ArticleJournal of gastroenterology2015
Epithelial-derived nuclear IL-33 aggravates inflammation in the pathogenesis of reflux esophagitis.
Article in Journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Pooled it
- The role of IL-33/ST2 axis in esophageal inflammatory diseases and cancers: implications for the immunopathogenesis and immunotherapeutic target?Therapeutic advances in gastroenterology · 2025Review
- Transcriptomic Insights into Hub Genes, Immune Infiltration, and Candidate Drugs in Erosive Esophagitis.Journal of inflammation research · 2024Article
- Unpacking the complexity of nuclear IL-33 (nIL-33): a crucial regulator of transcription and signal transduction.Journal of cell communication and signaling · 2023Review
- RNA-sequencing reveals molecular and regional differences in the esophageal mucosa of achalasia patients.Scientific reports · 2022Article
- Involvement of IL-33 in the Pathophysiology of Systemic Lupus Erythematosus: Review.International journal of molecular sciences · 2022Review
- IL-33 Participates in the Development of Esophageal Adenocarcinoma.Pathology oncology research : POR · 2022Article
- Identification of Unique Transcriptomic Signatures and Hub Genes Through RNA Sequencing and Integrated WGCNA and PPI Network Analysis in Nonerosive Reflux Disease.Journal of inflammation research · 2021Article
- Full-length IL-33 regulates Smad3 phosphorylation and gene transcription in a distinctive AP2-dependent manner.Cellular immunology · 2020Article
- A Phytocomplex Consisting ofOxidative medicine and cellular longevity · 2020Article
- Potent Potassium-competitive Acid Blockers: A New Era for the Treatment of Acid-related Diseases.Journal of neurogastroenterology and motility · 2018Review
- Cellular and clinicopathological features of the IL-33/ST2 axis in human esophageal squamous cell carcinomas.Cancer cell international · 2018Article
- IL-33/IL-31 Axis: A Potential Inflammatory Pathway.Mediators of inflammation · 2018Review
- Exploration of the Esophageal Mucosal Barrier in Non-Erosive Reflux Disease.International journal of molecular sciences · 2017Article
- Serotonin disrupts esophageal mucosal integrity: an investigation using a stratified squamous epithelial model.Journal of gastroenterology · 2016Article
- Contribution of immunomodulators to gastroesophageal reflux disease and its complications: stromal cells, interleukin 4, and adiponectin.Annals of the New York Academy of Sciences · 2016Review
- Gastrointestinal mucosal barrier function and diseases.Journal of gastroenterology · 2016Review
- Interleukin 33 is a guardian of barriers and a local alarmin.Nature immunology · 2016Review
- Article
- Interferon γ-Induced Nuclear Interleukin-33 Potentiates the Release of Esophageal Epithelial Derived Cytokines.PloS one · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIL-33 is a new tissue-derived cytokine constitutively expressed in epithelial cells and plays a role in sensing damage caused by inflammatory diseases. The function of IL-33 in the esophageal mucosa has not been previously described. Accordingly, we examined the expression of IL-33 and its role in the pathogenesis of reflux esophagitis (RE).
methodsIL-33 in the esophageal mucosa of RE patients and in an in vitro stratified normal esophageal squamous epithelial model was examined at the messenger RNA and protein levels. The correlation of the level of IL-33 and IL-8 or IL-6 was examined. Cell layers were stimulated with bile acids and cytokines. IL-33 was knocked down by small interfering RNA (siRNA). Pharmacological inhibitors and signal transducer and activator of transcription 1 (STAT1) siRNA were used.
resultsIL-33 was significantly upregulated in RE patients, and was located in the nuclei of basal and suprabasal layers. Upregulated IL-33 messenger RNA expression was correlated with IL-8 and IL-6 expression. In vitro, IL-33 was upregulated in the nuclei of basal and suprabasal layers by interferon-γ (IFNγ), and the upregulation was aggravated by the combination of deoxycholic acid (DCA) and IFNγ. IL-33 knockdown dampened IFNγ- and DCA-induced IL-8 and IL-6 production. IFNγ-induced IL-33 was inhibited by a Janus kinase inhibitor, a p38 mitogen-activated protein kinase inhibitor, and STAT1 siRNA.
conclusionsNuclear IL-33 is upregulated in erosive mucosa of RE patients and is correlated with IL-8 and IL-6 levels. The normal esophageal epithelial model enables us to show for the first time that epithelial-cell-derived nuclear but not exogenous IL-33 is located upstream of the production of inflammatory cytokines and can aggravate the inflammation.
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Registered trials
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