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Physical and immunological barrier of human primary nasal epithelial cells from non-allergic and allergic donors.
Bergougnan, Carolin; Dittlein, Daniela C; Hümmer, Elke; Riepl, Rosalie; Eisenbart, Selina; Böck, Dominik; Griesbaum, Lena; Weigl, Anna; Damialis, Athanasios; Hartwig, Alexander; Neumann, Avidan U; Zenk, Johannes; Traidl-Hoffmann, Claudia; Gilles, Stefanie.
Afiliação
  • Bergougnan C; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.
  • Dittlein DC; Christine-Kühne-Center for Allergy Research and Education (CK-Care), Davos, Switzerland.
  • Hümmer E; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.
  • Riepl R; Department of Otolaryngology, Augsburg University Medical School, 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; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.
  • Neumann AU; Institute of Physics, Augsburg University, Augsburg, Germany.
  • Zenk J; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.
  • Traidl-Hoffmann C; Department of Otolaryngology, Augsburg University Medical School, Augsburg, Germany.
  • Gilles S; Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and HelmholtzZentrum München, Augsburg, Germany.
World Allergy Organ J ; 13(3): 100109, 2020 Mar.
Article em En | MEDLINE | ID: mdl-32180893
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-1ß, 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-1ß). 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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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: World Allergy Organ J Ano de publicação: 2020 Tipo de documento: Article País de afiliação: Alemanha

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: World Allergy Organ J Ano de publicação: 2020 Tipo de documento: Article País de afiliação: Alemanha