MiR-31 attenuates murine allergic rhinitis by suppressing interleukin-13-induced nasal epithelial inflammatory responses.

Abstract

The present study aimed to investigate whether microRNA (miR)-31 exerted therapeutic potential in allergic rhinitis (AR) and to explore its underlying mechanism. Firstly, the expression levels of miR-31 were detected by reverse transcription-quantitative PCR in the nasal mucosa of patients and mice. Subsequently, an ovalbumin (OVA)-induced animal model of AR was constructed. Allergic symptom score, histopathological characteristics, OVA-specific immunoglobulin E (IgE) titers, and T-helper (Th)1 and Th2 cell-related cytokine levels were analyzed in OVA-sensitized mice, miR-31-overexpressing mice, miR-negative control mice and control mice. Furthermore, interleukin (IL)-13-stimulated nasal epithelial cells (NECs) were used to assess the effects of miR-31 on the production of IL-13-induced inflammatory cytokines and mucin 5AC by performing western blotting and ELISA. The expression levels of miR-31 were significantly decreased in the nasal mucosa of the AR group compared with those in the control group. Moreover, upregulation of miR-31 markedly attenuated sneezing and nasal rubbing events, reduced nasal eosinophil infiltration and goblet cell hyperplasia, and decreased the levels of OVA-specific IgE and Th2-related cytokines. In addition, subsequent in vitro experiments showed that upregulation of miR-31 inhibited IL-13 receptor α1 chain expression and signal transducer and activator of transcription 6 phosphorylation in NECs. Furthermore, miR-31 suppressed IL-13-induced expression of thymic stromal lymphopoietin, granulocyte-macrophage colony-stimulating factor, eotaxin and mucin 5AC in NECs. In conclusion, these data revealed that miR-31 could ameliorate AR by suppressing IL-13-induced nasal epithelial inflammatory responses, and thus may serve as a novel therapeutic target for AR.