ArticlePloS one2016
Specific Induction of TSLP by the Viral RNA Analogue Poly(I:C) in Primary Epithelial Cells Derived from Nasal Polyps.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- CRSwNP-derived cells retain native disease-relevant characteristics in vitro.Journal of inflammation (London, England) · 2026Article
- Thymic stromal lymphopoietin as a therapeutic target in patients with chronic rhinosinusitis and nasal polyps.Clinical and experimental immunology · 2025Review
- Thymic Stromal Lymphopoietin (TSLP): Evidence in Respiratory Epithelial-driven Diseases Including Chronic Rhinosinusitis with Nasal Polyps.Current allergy and asthma reports · 2024Review
- Multifactorial Causes and Consequences of TLSP Production, Function, and Release in the Asthmatic Airway.Biomolecules · 2024Review
- Cinnamaldehyde reduces inflammatory responses in chronic rhinosinusitis by inhibiting TRPM8 expression.American journal of translational research · 2024Article
- Developments in the Management of Severe Asthma in Children and Adolescents: Focus on Dupilumab and Tezepelumab.Paediatric drugs · 2023Review
- Tezepelumab Efficacy in Patients with Severe, Uncontrolled Asthma with Comorbid Nasal Polyps in NAVIGATOR.Journal of asthma and allergy · 2023Article
- CCL4 Functions as a Biomarker of Type 2 Airway Inflammation.Biomedicines · 2022Article
- Comprehensive Analysis of Nasal Polyps Reveals a More Pronounced Type 2 Transcriptomic Profile of Epithelial Cells and Mast Cells in Aspirin-Exacerbated Respiratory Disease.Frontiers in immunology · 2022Article
- TLR Signals in Epithelial Cells in the Nasal Cavity and Paranasal Sinuses.Frontiers in allergy · 2021Review
- Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells.Frontiers in cellular and infection microbiology · 2021Article
- Monoclonal Antibodies and Airway Diseases.International journal of molecular sciences · 2020Review
- Enhanced Type 2 Immune Reactions by Increased IL-22/IL-22Ra1 Signaling in Chronic Rhinosinusitis With Nasal Polyps.Allergy, asthma & immunology research · 2020Article
- Chronic Rhinosinusitis with Nasal Polyps: Targeting IgE with Anti-IgE Omalizumab Therapy.Drug design, development and therapy · 2020Review
- Release of Type 2 Cytokines by Epithelial Cells of Nasal Polyps.Journal of immunology research · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionChronic rhinosinusitis with nasal polyposis is an inflammatory disease that, although not directly linked to allergy, often displays a Th2-skewed inflammation characterized by elevated local IgE and IL-5 levels. The nasal cavity is constantly exposed to bacteria and viruses that may trigger epithelial inflammatory responses. To gain more insight into mechanisms by which such a biased inflammation might arise, we have investigated the epithelial expression of the Th2 skewing mediators (TSLP, IL-25, and IL-33) in relationship to disease and microbial triggers.
methodsEpithelial cells were obtained from polyp tissues of nasal polyposis patients and from inferior turbinates of non-diseased controls. Cells were exposed to various TLR-specific triggers to study the effect on mRNA and protein expression level of TSLP, IL-25, and IL-33 and the potential regulatory mechanisms through the expression profile the transcription factors ATF-3, DUSP-1, EGR-1, and NFKB-1.
resultsThe TLR3 agonist and viral analogue poly(I:C) induced TSLP mRNA 13.0 ± 3.1 fold (p < 0.05) and protein expression by 12.1 ± 2.3-fold (p < 0.05) higher in epithelium isolated from nasal polyposis patients than in epithelium form healthy controls. This enhanced induction of TSLP may be a consequence of a down-regulated expression of DUSP-1 in polyp epithelium.
conclusionThe TLR3 induced expression of TSLP introduces a mechanism by which the Th2-skewed tissue environment might arise in nasal polyps and invites a further evaluation of the potential contribution of current or past viral infections to polyposis pathogenesis.
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