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

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.