ArticleInternational forum of allergy & rhinology2014
Damage-associated molecular patterns stimulate interleukin-33 expression in nasal polyp epithelial cells.
Article in International forum of allergy & rhinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Sex-sikpecific associations between serum uric acid and chronic rhinosinusitis: a retrospective case-control study.Frontiers in allergy · 2026Article
- Comprehensive evaluation of type 2 endotype and clinical features in patients with chronic rhinosinusitis with nasal polyps in Taiwan: a cross-sectional study.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2023Article
- Interesting effects of interleukins and immune cells on acute respiratory distress syndrome.Clinical and experimental medicine · 2023Review
- Perspectives in Therapy of Chronic Rhinosinusitis.Diagnostics (Basel, Switzerland) · 2022Review
- Counteractive Effects of IL-33 and IL-37 on Inflammation in Osteoarthritis.International journal of environmental research and public health · 2022Article
- Eosinophils in the Field of Nasal Polyposis: Towards a Better Understanding of Biologic Therapies.Clinical reviews in allergy & immunology · 2022Review
- IL-33, IL-37, and Vitamin D Interaction Mediate Immunomodulation of Inflammation in Degenerating Cartilage.Antibodies (Basel, Switzerland) · 2021Article
- Role of P2X7R in eosinophilic and non‑eosinophilic chronic rhinosinusitis with nasal polyps.Molecular medicine reports · 2021Article
- Serum amyloid A is a soluble pattern recognition receptor that drives type 2 immunity.Nature immunology · 2020Article
- Contributions of Innate Lymphoid Cells in Chronic Rhinosinusitis.Current allergy and asthma reports · 2019Review
- Sentinels at the wall: epithelial-derived cytokines serve as triggers of upper airway type 2 inflammation.International forum of allergy & rhinology · 2019Review
- Interleukin-33 contributes to ILC2 activation and early inflammation-associated lung injury during abdominal sepsis.Immunology and cell biology · 2018Article
- Characterization of a novel, papain-inducible murine model of eosinophilic rhinosinusitis.International forum of allergy & rhinology · 2018Article
- Dysregulated invertebrate tropomyosin-dectin-1 interaction confers susceptibility to allergic diseases.Science immunology · 2018Article
- Oxygen matters: hypoxia as a pathogenic mechanism in rhinosinusitis.BMB reports · 2018Article
- HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature.International archives of otorhinolaryngology · 2017Review
- Cyclic stretch induced IL-33 production through HMGB1/TLR-4 signaling pathway in murine respiratory epithelial cells.PloS one · 2017Article
- Reversal of cigarette smoke extract-induced sinonasal epithelial cell barrier dysfunction through Nrf2 Activation.International forum of allergy & rhinology · 2016Article
- Innate Immune Responses to Fungal Allergens.Current allergy and asthma reports · 2016Review
- Interleukin 33 is a guardian of barriers and a local alarmin.Nature immunology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic rhinosinusitis with nasal polyps (CRSwNP) is a disorder characterized by eosinophilic inflammation and local T-helper 2 (Th2) cytokine production. Innate lymphoid cells that elaborate Th2 cytokines have recently been characterized within nasal polyps. These cells can be activated by the epithelial cell-derived cytokine interleukin-33 (IL-33). The objective of this study is to determine whether 2 molecules associated with tissue damage (high mobility group box-1 [HMGB-1] and adenosine triphosphate [ATP]) elicit expression of IL-33 in sinonasal epithelial cells (SNECs) derived from recalcitrant CRSwNP patients.
methodsEthmoid tissue was obtained from 8 recalcitrant CRSwNP and 9 control subjects during endoscopic sinus surgery (ESS). Tissue was prepared for immunohistochemistry and for SNEC air-liquid interface culture. After exposure to either HMGB1 or ATP in vitro, SNECs were processed for messenger RNA (mRNA) extraction and immunocytochemistry. IL-33 levels were determined by real-time polymerase chain reaction (PCR) and by immunochemical staining with anti-IL-33 antibody.
resultsIntranuclear IL-33 is normally expressed in basal epithelial cells, but is present in more apical cells and outside the nucleus in CRSwNP. Exposure of SNECs to HMGB-1 or ATP resulted in a statistically significant increase in IL-33 mRNA expression in SNECs derived from recalcitrant CRSwNP patients. This increase was reflected at the protein level by immunochemical staining of IL-33.
conclusionTissue damage is a nonspecific trigger of epithelial IL-33 production in treatment-recalcitrant polyps, which may be responsible for perpetuating eosinophilic inflammation in CRSwNP. This common pathway may help explain why multiple environmental and infectious agents have been implicated in CRSwNP exacerbation.
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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.