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微小RNA-20b促进哮喘小鼠中CD11b+Ly6G+Ly6C髓源性抑制细胞的积累。

MicroRNA-20b promotes the accumulation of CD11b+Ly6G+Ly6C myeloid-derived suppressor cells in asthmatic mice.

作者信息

Ma Hua, Guo Shujun, Luo Yulan, Wang Yimeng, Wang Helong, He Jing, Tang Jie, Shen Lin, Song Chuanwang

机构信息

Department of Immunology, Anhui Provincial Key Laboratory of Infection and Immunity, Bengbu Medical College, Bengbu, Anhui, China.

These authors contribute equally to this work.

出版信息

Cent Eur J Immunol. 2017;42(1):30-38. doi: 10.5114/ceji.2017.67316. Epub 2017 May 8.

Abstract

miR-20b is a member of the miR-106a-363 gene cluster, which has been shown to play an important role in a variety of diseases, including cancer, inflammation, and autoimmune diseases. Our previous study indicated that miR-20b has an inhibitory effect on airway inflammation in asthmatic mice, but the exact mechanism is unclear. In this study, we report that the ratio of CD11b+Ly6G+Ly6Clow cells, but not the amount of CD11b+Ly6C+Ly6G- cells, was increased in the lung tissue of asthmatic mice after intranasal instillation with miR-20b mimics, while Th2-type cytokines (interleukin (IL)-4 and IL-13) were significantly decreased in the bronchoalveolar lavage fluid. In addition, the transcription factor CREB regulated the expression of miR-20b. Our findings suggest that miR-20b can induce the accumulation of myeloid-derived suppressor cells in the lungs of asthmatic mice, which may be a mechanism by which miR-20b inhibits airway inflammation in asthmatic mice. Thus, miR-20b may be used as a target for the effective treatment of asthma in the future.

摘要

miR-20b是miR-106a-363基因簇的成员,该基因簇已被证明在包括癌症、炎症和自身免疫性疾病在内的多种疾病中发挥重要作用。我们之前的研究表明,miR-20b对哮喘小鼠的气道炎症有抑制作用,但其确切机制尚不清楚。在本研究中,我们报告称,经鼻滴注miR-20b模拟物后,哮喘小鼠肺组织中CD11b+Ly6G+Ly6Clow细胞的比例增加,而CD11b+Ly6C+Ly6G-细胞的数量未增加,同时支气管肺泡灌洗液中的Th2型细胞因子(白细胞介素(IL)-4和IL-13)显著减少。此外,转录因子CREB调节miR-20b的表达。我们的研究结果表明,miR-20b可诱导哮喘小鼠肺部髓源性抑制细胞的积累,这可能是miR-20b抑制哮喘小鼠气道炎症的一种机制。因此,miR-20b未来可能用作有效治疗哮喘的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2692/5470612/a05975141578/CEJI-42-29844-g001.jpg

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