Abstract
Purpose: Epidemiologic studies have reported that Asian sand dust (ASD) is associated with chronic inflammatory diseases of the respiratory system. Glucocorticoids (GCs) have potent anti-inflammatory properties. The aims of this study were to evaluate the effects of GCs on ASD-induced interleukin-32 (IL-32) expression and to identify the underlying signaling pathways in airway epithelial cells. Methods: A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to evaluate cytotoxicity in A549 and human primary nasal epithelial cells. Expression levels of IL-32 messenger RNA and protein were measured by Western blot, real-time polymerase chain reaction, ELISA, and immunofluorescence staining. Signaling pathways were analyzed using specific inhibitors of Akt, MAPK, or NF-κB. The effects of GCs on the expression of ASD-induced IL-32 were confirmed with ex vivo organ cultures of the nasal interior turbinate. Results: ASD (0–400 ng/mL) had no significant cytotoxic effects in A549 cells and human primary nasal epithelial cells. Expression levels of IL-32 were dose-dependently upregulated by ASD treatment in A549 cells. ASD induced phosphorylation of Akt, MAPK, and NF-κB, whereas GCs and specific inhibitors of Akt, MAPK, and NF-κB downregulated these activations and the expression of IL-32. These findings were further confirmed in human primary nasal epithelial cells and ex vivo organ cultures of the nasal interior turbinate. Conclusions: GCs have an inhibitory effect on ASD-induced IL-32 expression via the Akt, MAPK, and NF-κB signaling pathways in airway epithelial cells.
Original language | English |
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Pages (from-to) | 403-412 |
Number of pages | 10 |
Journal | American Journal of Rhinology and Allergy |
Volume | 33 |
Issue number | 4 |
DOIs | |
Publication status | Published - 2019 Jul 1 |
Keywords
- Asian sand dust
- epithelial cell
- glucocorticoid
- respiratory
- signaling pathway
ASJC Scopus subject areas
- Immunology and Allergy
- Otorhinolaryngology