Physical and immunological barrier of human primary nasal epithelial cells from non-allergic and allergic donors

Carolin Bergougnan, Daniela C. Dittlein, Elke Hümmer, Rosalie Riepl, Selina Eisenbart, Dominik Böck, Lena Griesbaum, Anna Weigl, Athanasios Damialis, Alexander Hartwig, Avidan U. Neumann, Johannes Zenk, Claudia Traidl-Hoffmann, Stefanie Gilles

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


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.

Original languageEnglish
Article number100109
JournalWorld Allergy Organization Journal
Issue number3
StatePublished - Mar 2020
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2020 The Author(s)


  • Allergic rhinitis
  • Inflammation
  • Nasal epithelium
  • Pattern recognition receptor
  • Pollen


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