Knockdown of DDX3Y alleviates ovalbumin-induced allergic rhinitis in mice by regulating NF-κB pathway.

Allergic rhinitis (AR), a type of chronic inflammatory disease that exists in the nasal mucosa, significantly impacts the quality of life. DDX3Y gene encodes an RNA helicase belonging to the DEAD-box protein family and is part of the DDX3 subfamily that affects the progression of multiple diseases. However, the specific role and mechanisms of DDX3Y in AR remain unclear. This study investigates the effects of DDX3Y knockdown on ovalbumin (OVA)-induced AR in mice. We found that DDX3Y is highly expressed in the nasal mucosa of AR mice. Knockdown of DDX3Y in OVA-induced AR mice significantly alleviated nasal manifestations, reduced immunoglobulin E and histamine levels, and improved nasal mucosal histopathology. Additionally, knockdown of DDX3Y suppressed secretion of inflammatory factor nuclear factor kappa B (NF-κB) phosphorylation, thereby mitigating local inflammatory responses. These findings suggested that targeting DDX3Y could offer a novel therapeutic strategy for managing AR by modulating the NF-κB pathway.