Abstract
Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by mucosal inflammation. Airborne allergens are associated with upper and lower airway inflammatory disease. We investigated the effects of airborne allergen stimulation in the nasal epithelial cells and their effect on the peripheral blood mononuclear cells’ (PBMCs) Th immune polarization. Interleukin (IL)-10, IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) levels were determined using the enzyme-linked immunosorbent assay (ELISA) in nasal polyp tissues. Cultured primary nasal epithelial cells were stimulated with Alternaria alternata, Aspergillus fumigatus, Dermatophagoides pteronyssinus (DP), and Dermatophagoides farina (DF) for 48 hours. IL-6, IL-25, IL-33, and TSLP production were measured by ELISA, and the nuclear factor-κB (NF-κB), activator protein 1 (AP-1), and mitogen-activated protein kinase (MAPK) expression were determined by western blot analyses. PBMCs were cultured with nasal epithelial cell-conditioned media (NECM), and IL-5, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α were measured. Innate lymphoid type2 cells (ILC2) were analyzed with flowcytometry. IL-25, IL-33, and TSLP levels were significantly higher in eosinophilic nasal polyps. Alternaria, DP, and DF enhanced IL-33 and TSLP production from the nasal epithelial cells through the NF-κB, AP-1, and MAPK pathway. NECM induced IL-5, IFN-γ, and TNF-α production from PBMCs, without increasing ILC2 expression. Alternaria and house dust mites enhanced the chemical mediator production from nasal epithelial cells and these allergens may induce not only Th2 inflammatory responses but also Th1 inflammatory responses in the nasal mucosa.
Highlights
Respiratory epithelial cells are the primary defense system against external pathogens with the initiation, maintenance, and regulation of innate and adaptive immune responses [1,2]
The results of this study demonstrated that Alternaria, and house dust mites (HDM) induced IL-33 and thymic stromal lymphopoietin (TSLP) production from nasal epithelial cells through the nuclear factor-κB (NF-κB), activator protein 1 (AP-1), and mitogen-activated protein kinase (MAPK) pathways
Alternaria-induced IL-33 and TSLP productions were significantly suppressed by NF-κB, AP-1, and MAPK inhibitors, HDM-induced TSLP production was not suppressed by the NF-κB inhibitor
Summary
Respiratory epithelial cells are the primary defense system against external pathogens with the initiation, maintenance, and regulation of innate and adaptive immune responses [1,2]. They play an important role in the inflammatory process of the respiratory mucosa with the production of chemical mediators. IL-25 belongs to the IL-17 cytokine family produced by T lymphocytes, dendritic cells, mast cells, basophils, eosinophils and epithelial cells [4]. TSLP is an IL-7 cytokine family, produced mainly by epithelial cells, epidermal keratinocytes, smooth muscle cells, fibroblasts, and dendritic cells. TSLP stimulates myeloid dendritic cells, leading to the differentiation of naïve T cells toward the Th2 cells [8]
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