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

Autor:	Bergougnan C; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.; Christine-Kühne-Center for Allergy Research and Education (CK-Care), Davos, Switzerland., Dittlein DC; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Hümmer E; Department of Otolaryngology, Augsburg University Medical School, Augsburg, Germany., Riepl R; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Eisenbart S; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Böck D; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Griesbaum L; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Weigl A; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Damialis A; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Hartwig A; Institute of Physics, Augsburg University, Augsburg, Germany., Neumann AU; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany., Zenk J; Department of Otolaryngology, Augsburg University Medical School, Augsburg, Germany., Traidl-Hoffmann C; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.; Christine-Kühne-Center for Allergy Research and Education (CK-Care), Davos, Switzerland., Gilles S; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.
Jazyk:	angličtina
Zdroj:	The World Allergy Organization journal [World Allergy Organ J] 2020 Mar 09; Vol. 13 (3), pp. 100109. Date of Electronic Publication: 2020 Mar 09 (Print Publication: 2020).
DOI:	10.1016/j.waojou.2020.100109
Abstrakt:	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. Competing Interests: All authors declare no conflict of interest and consent to the publication in its present form. (© 2020 The Author(s).)
Databáze:	MEDLINE
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