Inflammasome signalling pathway in the regulation of inflammation - its involvement in the development and exacerbation of asthma and chronic obstructive pulmonary disease.

IF 1.4 4区 医学 Q3 ALLERGY
Iga Panek, Maciej Liczek, Agata Gabryelska, Igor Rakoczy, Piotr Kuna, Michał Panek
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Abstract

Inflammasomes are multiprotein oligomers, whose main function is the recruitment and activation of caspase-1, which cleaves the precursor forms of interleukin (IL)-1β and IL-18, generating biologically active cytokines. Activation of inflammasome is an essential component of the innate immune response, and according to recent reports it is involved in epithelial homeostasis and type 2 T helper cell (Th2) differentiation. In recent years, the contribution of inflammasome dependent signalling pathways to the development of inflammatory diseases became a topic of multiple research studies. Asthma and chronic obstructive pulmonary disease (COPD) are the most prevalent obstructive lung diseases. Recent studies have focused on inflammatory aspects of asthma and COPD development, demonstrating the key role of inflammasome-dependent processes. Factors responsible for activation of inflammasome complex are similar in both asthma and COPD and include bacteria, viruses, cigarette smoke, and particulate matter. Some recent studies have revealed that NLRP3 inflammasome plays a crucial role, particularly in the development of acute exacerbations of COPD (AECOPD). Activation of NLRP3 inflammasome has been linked with neutrophilic severe steroid-resistant asthma. Although most of the studies on inflammasomes in asthma and COPD focused on the NLRP3 inflammasome, there are scarce scientific reports linking other inflammasomes such as AIM2 and NLRP1 with obstructive lung diseases. In this mini review we focus on the role of molecular pathways associated with inflammasome in the most prevalent lung diseases such as asthma and COPD. Furthermore, we will try to answer the question of whether inhibition of inflammasome can occur as a modern therapy in these diseases.

Abstract Image

Abstract Image

调节炎症的炎性小体信号通路-参与哮喘和慢性阻塞性肺疾病的发展和恶化。
炎性小体是一种多蛋白低聚体,其主要功能是募集和激活caspase-1, caspase-1可切割白介素(IL)-1β和IL-18的前体形式,产生具有生物活性的细胞因子。炎性小体的激活是先天免疫反应的重要组成部分,根据最近的报道,它参与上皮稳态和2型T辅助细胞(Th2)分化。近年来,炎性小体依赖信号通路在炎症性疾病发生发展中的作用成为众多研究的课题。哮喘和慢性阻塞性肺病(COPD)是最常见的阻塞性肺病。最近的研究集中在哮喘和慢性阻塞性肺病发展的炎症方面,证明了炎症小体依赖过程的关键作用。哮喘和慢性阻塞性肺病中导致炎性体复合体活化的因素相似,包括细菌、病毒、香烟烟雾和颗粒物。最近的一些研究表明,NLRP3炎性体在COPD急性加重(AECOPD)的发展中起着至关重要的作用。NLRP3炎性小体的激活与中性粒细胞性严重类固醇抵抗性哮喘有关。尽管大多数关于哮喘和COPD炎症小体的研究都集中在NLRP3炎症小体上,但将AIM2和NLRP1等其他炎症小体与阻塞性肺疾病联系起来的科学报道很少。在这篇综述中,我们关注与炎性小体相关的分子通路在最常见的肺部疾病如哮喘和COPD中的作用。此外,我们将尝试回答炎症小体抑制是否可以作为这些疾病的现代治疗方法的问题。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.60
自引率
7.10%
发文量
107
审稿时长
6-12 weeks
期刊介绍: Advances in Dermatology and Allergology/Postępy Dermatologii i Alergologii is a bimonthly aimed at allergologists and dermatologists.
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