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上皮细胞衍生的微小RNA-146a可产生分泌白细胞介素-10的单核细胞,以抑制鼻过敏。

Epithelial cell-derived micro RNA-146a generates interleukin-10-producing monocytes to inhibit nasal allergy.

作者信息

Luo Xi, Han Miaomiao, Liu Jianqi, Wang Yu, Luo Xiangqian, Zheng Jing, Wang Shuai, Liu Zhigang, Liu Dabo, Yang Ping-Chang, Li Huabin

机构信息

Department of Otolaryngology, Affiliated Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.

Department of Otolaryngology, Head and Neck Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

出版信息

Sci Rep. 2015 Nov 3;5:15937. doi: 10.1038/srep15937.

Abstract

The aberrant immunity plays an important role in the pathogenesis of allergic diseases. Micro RNAs (miR) are involved in regulating the immunity in the body. This study aims to test a hypothesis that miR-146a induces the expression of interleukin (IL)-10 in monocytes (Mos). In this study, the levels of miR-146a were determined by real time RT-PCR. The IL-10(+) Mos were evaluated by flow cytometry. The miR-146a-laden exosomes were generated with RPMI2650 cells (an airway epithelial cell line). An allergic rhinitis mouse model was developed. The results showed that nasal epithelial cells expressed miR-146a, which was markedly lower in the nasal epithelial cells of patients with nasal allergy than that in healthy controls. Exposure to T helper (Th)2 cytokines suppressed the levels of miR-146a in the nasal epithelial cells. The nasal epithelial cell-derived miR-146a up regulated the expression of IL-10 in Mos. The inducible IL-10(+) Mos showed an immune suppressor effect on the activities of CD4(+) effector T cells and the Th2 polarization in a mouse model of allergic rhinitis. In summary, nasal epithelial cells express miR-146a, the latter is capable of inducing IL-10 expression in Mos, which suppress allergic reactions in the mouse nasal mucosa.

摘要

异常免疫在过敏性疾病的发病机制中起重要作用。微小RNA(miR)参与调节机体免疫。本研究旨在验证一个假说,即miR-146a诱导单核细胞(Mos)中白细胞介素(IL)-10的表达。在本研究中,通过实时逆转录聚合酶链反应测定miR-146a的水平。通过流式细胞术评估IL-10(+)Mos。用RPMI2650细胞(一种气道上皮细胞系)产生携带miR-146a的外泌体。建立变应性鼻炎小鼠模型。结果显示,鼻上皮细胞表达miR-146a,其在鼻过敏患者的鼻上皮细胞中明显低于健康对照。暴露于辅助性T(Th)2细胞因子可抑制鼻上皮细胞中miR-146a的水平。鼻上皮细胞来源的miR-146a上调Mos中IL-10的表达。在变应性鼻炎小鼠模型中,诱导性IL-10(+)Mos对CD4(+)效应T细胞的活性和Th2极化显示出免疫抑制作用。总之,鼻上皮细胞表达miR-146a,后者能够诱导Mos中IL-10的表达,从而抑制小鼠鼻黏膜中的过敏反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5ac/4630644/6e5ee8d5bce6/srep15937-f1.jpg

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