Asian Sand Dust Regulates IL-32 Production in Airway Epithelial Cells: Inhibitory Effect of Glucocorticoids
- Authors
- Shin, Jae-Min; Kim, Hwee-in; Park, Joo-Hoo; Hwang, You Jin; Lee, Heung-Man
- Issue Date
- Jul-2019
- Publisher
- Oceanside Publications, Inc.
- Keywords
- Asian sand dust; epithelial cell; respiratory; signaling pathway; glucocorticoid
- Citation
- American Journal of Rhinology & Allergy, v.33, no.4, pp 403 - 412
- Pages
- 10
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- American Journal of Rhinology & Allergy
- Volume
- 33
- Number
- 4
- Start Page
- 403
- End Page
- 412
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/1875
- DOI
- 10.1177/1945892419839538
- ISSN
- 1945-8924
1945-8932
- 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-kappa B. 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-kappa B, whereas GCs and specific inhibitors of Akt, MAPK, and NF-kappa B 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-kappa B signaling pathways in airway epithelial cells.
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Collections - 4. Research institute > Institute for Medical Device Clinical Trial > 1. Journal Articles
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