Related Experiment Video
Updated: Jun 8, 2025
Author Spotlight: Advancing Allergic Rhinitis Research with Multicolor Immunofluorescence
Published on: September 22, 2023
Knockdown of DDX3Y alleviates ovalbumin-induced allergic rhinitis in mice by regulating NF-κB pathway
Ying Xu1, Xiaofeng Gu1, Jian Wu1
1Department of Otorhinolaryngology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu Province, China.
Abstract:
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.
Insights
This study reveals that the DDX3Y gene is highly expressed in allergic rhinitis (AR) and its knockdown alleviates AR symptoms by reducing inflammation via the NF-κB pathway.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Allergic rhinitis (AR) is a chronic nasal inflammatory disease impacting quality of life.
- The DDX3Y gene, encoding an RNA helicase, has an unclear role in AR pathogenesis.
- Understanding DDX3Y's function in AR is crucial for developing new treatments.
Purpose of the Study:
- To investigate the role and mechanism of DDX3Y in a mouse model of ovalbumin (OVA)-induced allergic rhinitis.
- To determine the effect of DDX3Y knockdown on AR-related symptoms and inflammatory pathways.
Main Methods:
- Induced AR in mice using ovalbumin (OVA) sensitization and challenge.
- Performed DDX3Y knockdown in the nasal mucosa of AR mice.
- Assessed nasal manifestations, immunoglobulin E (IgE) and histamine levels, and nasal mucosal histopathology.
- Analyzed the phosphorylation of nuclear factor kappa B (NF-κB) signaling pathway.
Main Results:
- DDX3Y was significantly upregulated in the nasal mucosa of AR mice.
- Knockdown of DDX3Y ameliorated nasal symptoms and reduced IgE and histamine levels.
- Histopathological examination showed improved nasal mucosa in DDX3Y-knockdown AR mice.
- DDX3Y knockdown suppressed NF-κB phosphorylation, indicating reduced local inflammation.
Conclusions:
- DDX3Y plays a significant role in the development of allergic rhinitis.
- Targeting DDX3Y, potentially through modulation of the NF-κB pathway, presents a novel therapeutic strategy for AR.
- Further research into DDX3Y's mechanisms could lead to effective AR treatments.
