Compared with controls, mRNA levels miR-155 (p<0.001), IL-25 (p<0.05), and IL-33 (p<0.001) were increased in nasal mucosa tissues of AR patients and AR mice, and ILC2s ratios were enhanced in human peripheral blood (p<0.0001), which were much higher after intranasal administration with miR-155 agomir (p<0.0001).
Although IL-33 did not induce the elevation of IL-4 production in the JCP-AR group, IL-33 substantially increased the production of IL-5 and IL-13 in comparison with antigen stimulation alone.
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.
AR mice shown significantly increased Th2 and Th17 cell ratio in spleen, IL-17 level in serum, IL-5 and IL-13 levels in NALF but a lower number of IL-33-positive epithelial cells and Th1 response (Th1 and Tbet<sup>+</sup>Th1 cell ratio in the spleen and serum IFN-γ level) than the control mice.1,25-(OH)<sub>2</sub>D<sub>3</sub> treatment significantly decreased the number of sneezing, nasal rubbing, OVA-sIgE and IL-17 in serum, IL-5 and IL-13 levels in NALF, Th17 cell ratio in the spleen and the histological of nasal mucosal but increased the number of IL-33-positive epithelial cells in AR mice.
In human subjects we revealed constitutive expression of IL-33 protein in the nasal epithelial cells of healthy control subjects and downregulated expression of IL-33 protein in inflamed nasal epithelial cells of patients with AR.
The aim of this study was to examine whether the serum IL-33 level and polymorphisms in IL-33 are associated with Japanese cedar (JC) pollinosis, the most common form of allergic rhinitis, and a major public health problem, in Japan.