Involvement of epigenetic modification in epithelial immune responses during respiratory syncytial virus infection

Involvement of epigenetic modification in epithelial immune responses during respiratory syncytial virus infection
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表观遗传修饰参与呼吸道合胞病毒感染期间上皮免疫反应

DOI:
10.1016/j.micpath.2019.03.019
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发表时间:
2019-05-01
影响因子:
3.8
通讯作者:
Qin Xiaoqun
Qin Xiaoqun
中科院分区:
医学3区
文献类型:
--
作者:
Liu Caixia;Xiang Yang;Qin Xiaoqun

文献摘要

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支气管上皮细胞(BEC)作为一个保护墙,对潜在的病原体和外来颗粒,控制呼吸道免疫反应的许多方面。BEC不仅作为气道的物理保护壁,而且作为先天性和适应性免疫应答的重要部分。呼吸道疾病的发生与多种上皮相关的通讯通路有关,这些通路由遗传和环境因素触发。表观遗传失调是一种潜在的机制,可能介导早期生活中的不良暴露,如严重感染和晚年的免疫功能缺陷。调节呼吸道内膜结构和作用的表观遗传因素也是评估呼吸道疾病易感性的一个有吸引力的领域。一些研究表明,上皮相关信号通路中的关键基因具有表观遗传修饰。介导RSV引起的严重细支气管炎与其在儿童期的不良后果之间关系的相互作用被广泛理解为免疫学性质,然而,尚未完全揭示。因此,我们的研究解释了上皮细胞的免疫作用和RSV通过表观遗传修饰引起的上皮细胞免疫失衡在气道高反应性机制中的作用。
The epithelial cells of bronchi (BECs) act as a protective wall against potential pathogens and foreign particles that controls many aspects of respiratory immune response. The BECs act as not only a physical protecting wall of the airways but also as a significant part of both the innate and adaptive immune responses. Many kind of epithelium-associated communicating pathways which are triggered by genetic and environmental causating agents get involved in development of respiratory tract abnormalities. Epigenetic dysregulation is one potential mechanism which may mediate between adverse in early life exposures such as severe infections and immunological function deficits in later life. Epigenetic factors which regulate the respiratory tract lining structure and role are also an attractive area to assess the susceptibility of respiratory tract diseases. Several studies show that the key genes in epithelium-related signaling pathways have epigenetic modifications. The interactions mediating the relationship between severe bronchiolitis caused by RSV and their adverse consequences in childhood are broadly understood as immunological in nature, however, are yet to be fully uncovered. Thus, our study explained the immune action of epithelium and RSV-triggered immune imbalance of epithelium through epigenetic modifications in the mechanism of airway hyperresponsiveness.