RBCK1 Overexpression Attenuates Inflammation and Mobility of Derp1-Induced Nasal Mucosal Cells by Downregulating NLRP3.

INTRODUCTION: Allergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa, the incidence of which can reach 10-30% worldwide. RBCK1 (RANBP2-type and C3HC4-type zinc finger-containing 1) is a protein found in nasal epithelial cells; however, its function is not fully understood.

METHODS: In this study, RT-qPCR and Western blotting were used to detect RBCK1 expression in the nasal epithelial tissues of AR and non-AR patients. Next, an AR cell model was established by using the house dust mite allergen (Derp1), and the model cells were then transfected with RBCK1 or NLRP3 overexpression plasmids. Subsequently, RBCK1 expression was detected, and IL-18, IL-33, and LDH levels were determined with ELISA kits. NF-κB and p-NF-κB expression was monitored by Western blotting, and cell migration and invasion were assessed by transwell assays.

RESULTS: Our results showed that the AR model cells were successfully created by Derp1 stimulation and that BCK1 was expressed at low levels in the nasal epithelial tissues of AR patients and AR model cells. We also found that overexpression of RBCK1 could prevent inflammation and the migration and invasion of Derp1-mediated AR model cells. Moreover, NLRP3 was found to help prevent RBCK1 overexpression during the inflammation and mobility of AR model cells.

CONCLUSIONS: RBCK1 overexpression suppressed the inflammatory and mobility progression of AR model cells by downregulating NLRP3. Our data suggest RBCK1 as an important target for AR therapy.