MicroRNA-345-5p acts as an anti-inflammatory regulator in experimental allergic rhinitis via the TLR4/NF-κB pathway

被引:25
作者
Liu, Jie [1 ]
Jiang, Yan [1 ]
Han, Min [1 ]
Jiang, Liwei [1 ]
Liang, Dapeng [1 ]
Li, Shenling [1 ]
Xu, Zhenju [1 ]
Wang, Lin [1 ]
Li, Na [1 ]
机构
[1] Qingdao Univ, Affiliated Hosp, Dept Otorhinolaryngol Head & Neck Surg, 16 Jiangsu Rd, Qingdao 266000, Shandong, Peoples R China
关键词
MicroRNA-345-5p; TLR4/NF-kappa B pathway; Allergic rhinitis; Inflammatory response; Anti-inflammatory effect; TOLL-LIKE RECEPTORS; EXPRESSION PROFILES; INFLAMMATION; TH1/TH2;
D O I
10.1016/j.intimp.2020.106522
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Allergic rhinitis (AR) is a common chronic condition characterized by inflammation of the nasal mucosa. The correlation of microRNAs (miRNAs) in AR has been highlighted particularly due to their roles in regulating inflammatory responses. The aim of this study was to explore the anti-inflammatory mechanism by which miR-345-5p regulates the toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-kappa B) pathway in mice with AR. Initially, the putative miR-345-5p binding sites on the 3'untranslated region of TLR4 was predicted and verified. AR models were established using ovalbumin, after which the functional role of miR-345-5p in AR was determined using gain- and loss-of-function approaches. We found that miR-345-5p was poorly expressed in nasal mucosal tissues of mice with AR. Meanwhile, TLR4 expression and the TLR4/NF-kappa B pathway were identified to be promoted, which were then suppressed in the presence of overexpressed miR-345-5p. In addition, nasal epithelial cell apoptosis and fibrosis were inhibited in response to miR-345-5p overexpression and TLR4 silencing. Furthermore, miR-345-5p overexpression and TLR4 silencing were observed to decrease Th2 cells, expression of pro-inflammatory factors, but to increase Th1 cells and expression of anti-inflammatory factors. This study demonstrates an important role of miR-345-5p in alleviating the inflammatory response in mice with AR by inhibiting the TLR4/NF-kappa B pathway. Therefore, a better understanding of this process may aid in the development of novel therapeutic agents of AR.
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页数:9
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