Abstract

Allergic rhinitis (AR) is one of the most common chronic diseases. This study examined whether microRNA (miR)-182-5p plays a role in AR by regulating toll-like receptor 4 (TLR4). First, data demonstrated that TLR4 was a target of miR-182-5p. Subsequently, AR mouse model was established to explore the role of miR-182-5p and TLR4 in AR in vivo. Initially, quantitative reverse transcription-PCR (qRT-PCR) analysis indicated that miR-182-5p was downregulated, while TLR4 expression was upregulated in AR mice. Then we found that miR-182-5p mimic reduced the frequency of sneezing and nose rubbing of the AR mice. In addition, miR-182-5p mimic significantly increased ovalbumin (OVA)-specific IgE and leukotriene C4 expression levels in nasal lavage fluid (NLF) and serum of AR mice. miR-182-5p mimic decreased the number of inflammatory cells in NLF of AR mice. It also reduced the levels of inflammatory factors in the serum of AR mice, such as interleukin (IL)-4, IL-5, IL-13, IL-17 and tumor necrosis factor (TNF)-α, while increasing the release of IFN-γ and IL-2. Finally, miR-182-5p mimic inhibited NF-κB signaling pathway activation in AR mice. However, all effects of miR-182-5p mimic on AR mice were reversed by TLR4-plasmid. In conclusion, miR-182-5p/TLR4 axis may represent a novel therapeutic target for AR.

Highlights

  • Allergic rhinitis (AR) is one of the most common chronic diseases

  • The underlying mechanism of toll-like receptor 4 (TLR4) in AR was examined by the bioinformatic prediction algorithm TargetScan

  • The results indicated that TLR4 may be a target gene downstream of miR-182-5p (Figure 1a)

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Summary

Introduction

Allergic rhinitis (AR) is one of the most common chronic diseases. Its main feature is nasal mucositis, which is the most common non-infectious rhinitis driven by an immune response mediated by immunoglobulin E (IgE) [1]. AR induces upper respiratory tract inflammation, which is associated with release of mediators by several types of hypersensitive immune cells, including antigenpresenting cells, eosinophils, B cells and mast cells [2]. AR disease has affected social life and caused significant economic burden to families [1]. It has reduced the quality of life of patients [1]. With the advancement of medical treatment, several therapeutic options have emerged for AR, including intranasal steroids, antihistamines, leukotriene receptor antagonists and immunotherapy [4,5]. The treatment options for 20% of AR patients remain suboptimal [6]. A novel approach has to be developed for the effective treatment of AR

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