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Mast cell (MC) degranulation is the foundation of the acute phase of allergic rhinitis (AR). Previously, downregulation of GATA binding protein 3 (GATA-3) was shown to suppress MC activation in an AR mouse model. Binding of microRNA-135a (miR-135a) to GATA-3 was also observed, and overexpression of this miRNA decreased GATA-3 mRNA and protein expression. However, the effects of miR-135a on MCs during AR are currently unknown. In the present study, we utilized a lentiviral (LV) vector to intranasally administer miR-135a to ovalbumin (OVA)-sensitized AR mice. Following miR-135a treatment, the total serum IgE concentration observed during AR was significantly reduced. In the nasal mucosa, the expression of T-box expressed in T cells (T-bet) was higher, whereas that of GATA-3 was lower in the AR mice following miRNA treatment. Notably, during AR, the ratio of type 1 T-helper cells (Th1) to type 2 (Th2) cells in the spleen is unbalanced, favoring Th2. However, administering miR-135a to the AR mice appeared to balance this ratio by increasing and decreasing the percentage of Th1 and Th2 cells, respectively. MiR-135a also appeared to strongly suppress the infiltration of eosinophils and MCs into the nasal mucosa, and it was specifically localized in the MCs, suggesting that its influence is modulated through regulation of GATA-3 in these cells. Additional work identifying the full therapeutic potential of miR-135a in the treatment of AR and diseases involving allergen-induced inflammation is warranted.

BackgroundInterleukin-10 (IL-10) has an important anti-inflammatory and immunoregulatory function, and its expression is negatively correlated with the development and severity of allergic rhinitis (AR). However, the in vivo effects of exogenous IL-10 on AR have not been studied and the mechanisms underlying the effects of IL-10 have not been fully understood. Here, we investigated the effects of intranasal administration of recombinant mouse (rm) IL-10 on the expression of Th responses and local IL-10 in a mouse model of AR induced by ovalbumin.ResultsAdministration of rmIL-10 during challenge significantly reduced the number of eosinophils and mast cells, as well as Type 2 helper T (Th2) and Th17 cell related cytokine and transcription factor levels in the nasal mucosa and nasal lavage fluid in AR mice. The rmIL-10 treatment significantly inhibited the number of IL-10-positive cells and IL-10 mRNA expression in the nasal mucosa in AR mice.ConclusionOur results show that exogenous IL-10 administrated in challenge phase alleviates nasal allergic inflammation in AR mice, most likely by inhibiting Th2 and Th17 responses. It can also inhibit local IL-10 levels in the nasal mucosa. Our findings indicate that IL-10 may have the potential as an inhibitor of AR.