%0 Journal Article
%T Asian Sand Dust Regulates IL
%A Heung-Man Lee
%A Hwee-Jin Kim
%A Jae-Min Shin
%A Joo-Hoo Park
%A You Jin Hwang
%J American Journal of Rhinology & Allergy
%@ 1945-8932
%D 2019
%R 10.1177/1945892419839538
%X 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. 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-百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. ASD (0每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-百B, whereas GCs and specific inhibitors of Akt, MAPK, and NF-百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. GCs have an inhibitory effect on ASD-induced IL-32 expression via the Akt, MAPK, and NF-百B signaling pathways in airway epithelial cells
%K Asian sand dust
%K epithelial cell
%K respiratory
%K signaling pathway
%K glucocorticoid
%U https://journals.sagepub.com/doi/full/10.1177/1945892419839538