ASD profoundly affects respiratory health by inducing inflammation and causing upper airway inflammatory diseases. The impact of ASD on the production of IL-6 and IL-8 in nasal fibroblasts remains underexamined. The researchers investigated the impact of ASD on the induction of pro-inflammatory mediators and its underlying mechanisms in nasal fibroblasts.

Real-time cytotoxicity assays were used to determine the effect of ASD on the viability of fibroblasts. Researchers performed Enzyme-linked immunosorbent assays and real-time polymerase chain reactions to determine whether ASD induced the expression of IL-6 and IL-8. ROS was quantified using 2, 7-dichlorofluorescein-diacetate, and MitoSOX Red. Induction of IL-6 and IL-8 signal transduction pathways by ASD was confirmed by Western blotting. Ex vivo culture of the inferior turbinate tissue was performed to verify the effects of ASD.

ASD promoted IL-6 and IL-8 expression through the MAPK and CREB signaling pathways in nasal fibroblasts. However, ASD did not induce phosphorylation of p38. Specific inhibitors of each path suppressed ASD-induced IL-6 and IL-8 upregulation.

The study concluded that ASD induces pro-inflammatory mediators, and the increased levels of IL-6 and IL-8 might be associated with the pathogenesis of chronic rhinosinusitis.