ArticleAmerican journal of rhinology & allergy
Treatment-recalcitrant chronic rhinosinusitis with polyps is associated with altered epithelial cell expression of interleukin-33.
Article in American journal of rhinology & allergy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 118 citations in OpenAlex.
- Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene-Driven IL-33-Mediated Mast Cell Activation Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2015Trial
- Tissue Interleukin-33: A Novel Potential Regulator of Innate Immunity and Biomarker of Disease Severity in Chronic Rhinosinusitis with Nasal Polyps.Journal of clinical medicine · 2023Article
- The Diagnostic and Prognostic Role of Biomarkers in Chronic Rhinosinusitis.Diagnostics (Basel, Switzerland) · 2023Review
- Management of Patients with Severe Asthma and Chronic Rhinosinusitis with Nasal Polyps: A Multidisciplinary Shared Approach.Journal of personalized medicine · 2022Review
- Serum IL-5, POSTN and IL-33 levels in chronic rhinosinusitis with nasal polyposis correlate with clinical severity.BMC immunology · 2022Article
- Allergo Journal : interdisziplinare Zeitschrift fur Allergologie und Umweltmedizin : Organ der Deutschen Gesellschaft fur Allergie- und Immunitatsforschung · 2022Review
- ILCs and Allergy.Advances in experimental medicine and biology · 2022Article
- Strong correlation between air-liquid interface cultures and in vivo transcriptomics of nasal brush biopsy.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Recent advances in mast cell activation and regulation.F1000Research · 2020Review
- Group 2 Innate Lymphoid Cells in Human Respiratory Disorders.Journal of innate immunity · 2020Review
- Sentinels at the wall: epithelial-derived cytokines serve as triggers of upper airway type 2 inflammation.International forum of allergy & rhinology · 2019Review
- [Immunology of chronic rhinosinusitis with nasal polyps as a basis for treatment with biologicals].HNO · 2019Review
- Solitary chemosensory cells are a primary epithelial source of IL-25 in patients with chronic rhinosinusitis with nasal polyps.The Journal of allergy and clinical immunology · 2018Article
- Interleukin-33: Its Emerging Role in Allergic Diseases.Molecules (Basel, Switzerland) · 2018Review
- Pathogenesis of Recalcitrant Chronic Rhinosinusitis: The Emerging Role of Innate Immune Cells.Immune network · 2018Review
- Type 2 Cysteinyl Leukotriene Receptors Drive IL-33-Dependent Type 2 Immunopathology and Aspirin Sensitivity.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Subtyping of polyposis nasi: phenotypes, endotypes and comorbidities.Allergo journal international · 2018Review
- Contemporary Pharmacotherapy for Allergic Rhinitis and Chronic Rhinosinusitis.Otolaryngologic clinics of North America · 2017Review
- Biomarkers in the evaluation and management of chronic rhinosinusitis with nasal polyposis.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 · 2017Review
- IL-33: biological properties, functions, and roles in airway disease.Immunological reviews · 2017Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAbnormalities in host mucosal immunity exist in chronic rhinosinusitis with nasal polyps (CRSwNPs), but it is unclear whether this is a cause or an effect of the eosinophilic inflammation and frequent microbial colonization that characterizes the disease. Sinonasal epithelial cells (SNECs) are critical participants in healthy antimicrobial innate immune defense. They also can promote Th2 inflammation with various mediators, including interleukin (IL)-33, which induces T helper cells to produce Th2 cytokines.
methodsCRSwNP SNECs were obtained during sinus surgery and stored. Patients were subsequently classified as either treatment responsive or treatment recalcitrant, based on long-term outcomes of medical and surgical therapy. Epithelial cells from these patients were grown in air-liquid interface (ALI) culture and treated with IL-13, as well as the bacteria-associated molecule, CpG. Expression of IL-33 mRNA was determined by real-time polymerase chain reaction.
resultsRecalcitrant CRSwNP epithelial cells had increased baseline expression of IL-33 compared with responsive CRSwNPs, which was further increased by 24-hour exposure to CpG. Treatment-responsive epithelial cells were not induced by CpG to express IL-33. Prolonged treatment with IL-13 during differentiation at the ALI diminished the baseline expression of IL-33 and prevented the subsequent induction of IL-33 by CpG.
conclusionMucosal innate immunity likely plays an important role in CRSwNP pathogenesis. A definitive link between infectious triggers and the development of Th2 inflammation has been elusive. We have found constitutive IL-33 expression by SNECs in recalcitrant CRSwNPs, which can be further induced by a bacteria-associated molecular pattern. Dysregulated epithelial cell immune interactions between host and environment may contribute to Th2 inflammation in CRSwNPs.
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