MiR-487b mitigates allergic rhinitis through inhibition of the IL-33/ST2 signaling pathway.

Abstract

To investigate the potential effect of miR-487b/IL-33-ST2 axis on the pathology of allergic rhinitis (AR) and the relevant mechanism. The expression level of interleukin-33 (IL-33), a homolog of sulfotransferase (ST2), and miR-487b were detected in patients with or without allergic rhinitis. Luciferase assay was performed to evaluate the interaction between miR-487b and IL-33, and the effects of miR-487b/IL-33-ST2 axis on allergic rhinitis mice were determined by established allergic rhinitis model in mice by ovalbumin (OVA). The levels of OVA-specific immunoglobulin E (Ig-E), proinflammatory cytokines (IL-4, IL-5, and IL-13), and pathological alterations were detected. The level of IL-33 and its specific ligand ST2 were found increased in allergic rhinitis patients while miR-487b expression level was markedly repressed. To confirm whether miR-487b has a regulation effect on IL-33, we checked it in three publicly available algorithms, TargetScan, miRDB, and microRNA. We found that IL-33 is a direct target of miR-487b, and Luciferase assays confirmed our hypothesis, the subsequent experiments showed that up-regulation of miR-487b could inhibit expression of IL-33 and ST2, resulting in the decrease of the immunoglobulin E (Ig-E), proinflammatory cytokines and mitigation of pathological alterations. Our research discovered the suppressor function of miR-487b in allergic rhinitis and revealed that miR-487b/IL-33-ST2 axis may be a potential therapeutic target for the treatment of allergic rhinitis.