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基因多态性及其在哮喘和慢性阻塞性肺疾病炎症反应调节中的作用。

Genetic polymorphisms and their involvement in the regulation of the inflammatory response in asthma and COPD.

作者信息

Reséndiz-Hernández Juan M, Falfán-Valencia Ramcés

机构信息

HLA Laboratory, National Institute of Respiratory Diseases Ismael Cosio Villegas, Mexico City, Mexico.

Graduate Program in Biological Sciences, National Autonomous University of Mexico, Mexico City, Mexico.

出版信息

Adv Clin Exp Med. 2018 Jan;27(1):125-133. doi: 10.17219/acem/65691.

DOI:10.17219/acem/65691
PMID:29521053
Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are widely documented diseases with an inflammatory component. Asthma is a heterogeneous disorder of the airways that involves chronic inflammation, decline of the airway function and tissue remodeling. Chronic obstructive pulmonary disease is a preventable and treatable disease, which is characterized by persistent limited airflow, and is usually progressive with an increased inflammatory response in the airways. The inflammatory response is evoked by the stimulus of noxious particles and gases. Inflammation is a natural process in response to injury, but in asthma and COPD patients it occurs as an abnormal immune response to pathogenic stimuli which induce chronic inflammation, a key process in the pathogenesis of both diseases. However, the inflammatory process is different in both diseases, and is involved in several release patterns of inflammation mediators. It is not entirely clear whether these proteins are simply markers of the inflammatory process that accompanies a chronic disease or if they play a major role in the pathogenesis of the disease. The main proteins which have been described in these illnesses are: IL-4, IL-6, IL-8, and TNF-α. In addition, polymorphisms have been described in genes encoding these proteins that alter the transcription and susceptibility associated with these diseases. In this review, we will focus on asthma and COPD, and the involvement of these proteins and their genetic polymorphisms.

摘要

哮喘和慢性阻塞性肺疾病(COPD)是有炎症成分的广泛记载的疾病。哮喘是一种气道的异质性疾病,涉及慢性炎症、气道功能下降和组织重塑。慢性阻塞性肺疾病是一种可预防和可治疗的疾病,其特征是气流持续受限,通常呈进行性发展,气道炎症反应增加。炎症反应由有害颗粒和气体的刺激引起。炎症是对损伤的一种自然反应过程,但在哮喘和COPD患者中,它作为对致病刺激的异常免疫反应而发生,这种刺激会诱发慢性炎症,这是两种疾病发病机制中的关键过程。然而,两种疾病中的炎症过程不同,且涉及多种炎症介质的释放模式。这些蛋白质究竟只是伴随慢性病的炎症过程的标志物,还是在疾病发病机制中起主要作用,目前尚不完全清楚。在这些疾病中已被描述的主要蛋白质有:白细胞介素-4(IL-4)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)和肿瘤坏死因子-α(TNF-α)。此外,已在编码这些蛋白质的基因中描述了多态性,这些多态性会改变与这些疾病相关的转录和易感性。在本综述中,我们将重点关注哮喘和COPD,以及这些蛋白质及其基因多态性的影响。

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