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 |
|---|---|
| Journal | American Journal of Rhinology and Allergy |
| DOIs | |
| Publication status | Published - 2019 Jan 1 |
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Keywords
- Asian sand dust
- epithelial cell
- glucocorticoid
- respiratory
- signaling pathway
ASJC Scopus subject areas
- Immunology and Allergy
- Otorhinolaryngology
Cite this
Asian Sand Dust Regulates IL-32 Production in Airway Epithelial Cells : Inhibitory Effect of Glucocorticoids. / Shin, Jae Min; Kim, Hwee Jin; Park, Joo Hoo; Hwang, You Jin; Lee, Heung Man.
In: American Journal of Rhinology and Allergy, 01.01.2019.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Asian Sand Dust Regulates IL-32 Production in Airway Epithelial Cells
T2 - Inhibitory Effect of Glucocorticoids
AU - Shin, Jae Min
AU - Kim, Hwee Jin
AU - Park, Joo Hoo
AU - Hwang, You Jin
AU - Lee, Heung Man
PY - 2019/1/1
Y1 - 2019/1/1
N2 - 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.
AB - 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.
KW - Asian sand dust
KW - epithelial cell
KW - glucocorticoid
KW - respiratory
KW - signaling pathway
UR - http://www.scopus.com/inward/record.url?scp=85063566161&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85063566161&partnerID=8YFLogxK
U2 - 10.1177/1945892419839538
DO - 10.1177/1945892419839538
M3 - Article
C2 - 30919652
AN - SCOPUS:85063566161
JO - American Journal of Rhinology and Allergy
JF - American Journal of Rhinology and Allergy
SN - 1945-8924
ER -