Epidemiologic studies have reported that ASD is associated with chronic inflammatory diseases of the respiratory system. GCs have potent anti-inflammatory properties. This study aimed to evaluate the effects of expression and 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. 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.

ASD 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. These findings were further confirmed in human primary nasal epithelial cells and ex vivo organ cultures of the nasal interior turbinate.

The study concluded that GCs have an inhibitory effect on ASD-induced IL-32 expression via the Akt, MAPK, and NF-κB signaling pathways in airway epithelial cells.

Reference: https://journals.sagepub.com/doi/full/10.1177/1945892419839538