Physical and immunological barrier of human primary nasal epithelial cells from non-allergic and allergic donors.
ALI, Air liquid interphase
APE, Aqueous pollen extract
AR, Allergic rhinitis
Allergic rhinitis
HDM, House dust mite
HNEC, Human nasal epithelial cell
Inflammation
LPS, Lipopolysaccharide from E. Coli K12 (TLR-4 ligand)
MyD88, Myeloid differentiation primary response 88
Nasal epithelium
PAMP, Pathogen-associated molecular pattern
PRR, Pattern recognition receptor
Pattern recognition receptor
Pollen
PolyIC, Polyinosinic–polycytidylic acid (TLR-3 ligand)
SAR, Seasonal allergic rhinitis
SEM, Scanning electron microscopy
TER, Transepithelial electrical resistance
TLR, Toll-like receptor
TRIF, TIR-domain-containing adapter-inducing interferon-β
Journal
The World Allergy Organization journal
ISSN: 1939-4551
Titre abrégé: World Allergy Organ J
Pays: United States
ID NLM: 101481283
Informations de publication
Date de publication:
Mar 2020
Mar 2020
Historique:
received:
25
07
2019
revised:
04
12
2019
accepted:
12
02
2020
entrez:
18
3
2020
pubmed:
18
3
2020
medline:
18
3
2020
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 32180893
doi: 10.1016/j.waojou.2020.100109
pii: S1939-4551(20)30012-0
pii: 100109
pmc: PMC7063333
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100109Informations de copyright
© 2020 The Author(s).
Déclaration de conflit d'intérêts
All authors declare no conflict of interest and consent to the publication in its present form.
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