ArticleThe World Allergy Organization journal2020
Physical and immunological barrier of human primary nasal epithelial cells from non-allergic and allergic donors.
Article in The World Allergy Organization journal, 2020. 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, 42 citations in OpenAlex.
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- Advances in molecular innate immune regulation in the development and therapeutic strategies of allergic rhinitis vaccines.Frontiers in immunology · 2026Review
- HDAC8 impairs tight junctions in allergic rhinitis through Smad7 deacetylation.Frontiers in immunology · 2026Article
- Promising Cancer Vaccine for Glioblastoma Therapy: A Focus on mRNA Vaccine.Cancer medicine · 2025Review
- Research progress of mRNA vaccines for infectious diseases.European journal of medical research · 2025Review
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- miR-6089 Alleviates Inflammation and Cell Apoptosis Through Modulating the TLR4 Pathway in Mite-Sensitized Allergic Rhinitis.Journal of inflammation research · 2025Article
- Regulation of Airway Epithelial-Derived Alarmins in Asthma: Perspectives for Therapeutic Targets.Biomedicines · 2024Review
- Bioengineering Human Upper Respiratory Mucosa: A Systematic Review of the State of the Art of Cell Culture Techniques.Bioengineering (Basel, Switzerland) · 2024Review
- Airborne pollen exposure and risk of hospital admission for allergic rhinitis in Beijing: A time-stratified case-crossover study.Clinical and translational allergy · 2024Article
- IL-1Mediators of inflammation · 2023Review
- Birch pollen-The unpleasant herald of spring.Frontiers in allergy · 2023Review
- Common Pollen Modulate Immune Responses against Viral-Like Challenges in Airway Coculture Model.Journal of immunology research · 2023Article
- Neuroimmune communication in allergic rhinitis.Frontiers in neurology · 2023Review
- Downregulation of deubiquitinating enzyme USP25 promotes the development of allergic rhinitis by enhancing TSLP signaling in the nasal epithelium.Molecular medicine reports · 2022Article
- How Do Pollen Allergens Sensitize?Frontiers in molecular biosciences · 2022Review
- Nasal Cytology: A Easy Diagnostic Tool in Precision Medicine for Inflammation in Epithelial Barrier Damage in the Nose. A Perspective Mini Review.Frontiers in allergy · 2022Review
- Higher airborne pollen concentrations correlated with increased SARS-CoV-2 infection rates, as evidenced from 31 countries across the globe.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- mRNA vaccine: a potential therapeutic strategy.Molecular cancer · 2021Review
- Der p 1 Disrupts the Epithelial Barrier and Induces IL-6 Production in Patients With House Dust Mite Allergic Rhinitis.Frontiers in allergy · 2021Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial cell-derived cytokine milieu has been discussed as a "master switch" in the development of allergic disease. To understand the role of innate immune response in nasal epithelial cells during allergic inflammation, we created and established a fast and minimally invasive method to isolate and culture human nasal epithelial cells from clinically and immunologically well characterized patients. Human nasal epithelial cells from non-atopic volunteers and from allergic rhinitis patients were compared in respect to their growth, barrier integrity, pattern recognition, receptor expression, and immune responses to allergens and an array of pathogen-associated molecular patterns and inflammasome activators. Cells from nasal scrapings were clearly identified as nasal epithelial cells by staining of pan-Cytokeratin, Cytokeratin-14 and Tubulin. Additionally, Mucin 5AC staining revealed the presence of goblet cells, while staining of tight-junction protein Claudin-1, Occludin and ZO-1 showed the ability of the cells to form a tight barrier. Cells of atopic donors grew slower than cells of non-atopic donors. All nasal epithelial cells expressed TLR1-6 and 9, yet the expression of TLR-9 was lower in cells from allergic rhinitis (AR) donors. Additionally, epithelial cells from AR donors responded with a different TLR expression pattern to stimulation with TLR ligands. TLR-3 was the most potent modulator of cytokine and chemokine secretion in all human nasal epithelial cells (HNECs). The secretion of IL-1β, CCL-5, IL-8, IL-18 and IL-33 was elevated in HNECs of AR donors as compared to cells of non-atopic donors. This was observed in the steady-state (IL-18, IL-33) as well as under stimulation with TLR ligands (IL-18, IL-33, CCL-5, IL-8), aqueous pollen extracts (IL-18, IL-33), or the inflammasome activator Nigericin (IL-1β). In conclusion, nasal epithelial cells of AR donors show altered physical barrier responses in steady-state and in response to allergen stimulation. Cells of AR donors show increased expression of pro-inflammatory and IL-1 family cytokines at baseline and under stimulation, which could contribute to a micromilieu which is favorable for Th2.
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