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The NLRP3 inflammasome: Role in airway inflammation

机译：NLRP3炎性体：在气道炎症中的作用

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摘要

Asthma is characterized by airway inflammation, airway hyperresponsiveness and airway remodelling. Uncontrolled airway inflammation or repeated asthma exacerbations can lead to airway remodelling, which cannot be reversed by current pharmacological treatment, and consequently lead to decline in lung function. Thus, it is critical to understand airway inflammation in asthma and infectious exacerbation. The inflammasome has emerged as playing a key role in innate immunity and inflammation. Upon ligand sensing, inflammasome components assemble and self-oligomerize, leading to caspase-1 activation and maturation of pro-IL-1β and pro-IL-18 into bioactive cytokines. These bioactive cytokines then play a pivotal role in the initiation and amplification of inflammatory processes. In addition to facilitating the proteolytic activation of IL-1β and IL-18, inflammasomes also participate in cell death through caspase-1-mediated pyroptosis. In this review, we describe the structure and function of the inflammasome and provide an overview of our current understanding of role of the inflammasome in airway inflammation. We focus on nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome as it is the best-characterized subtype shown expressed in airway and considered to play a key role in chronic airway diseases such as asthma.
机译：哮喘的特征是气道炎症，气道高反应性和气道重塑。不受控制的气道炎症或反复发作​​的哮喘可导致气道重塑，目前的药物治疗无法逆转，从​​而导致肺功能下降。因此，了解哮喘和感染加重期的气道炎症至关重要。炎症小体已经在先天免疫和炎症中起关键作用。配体感应后，炎症小体成分组装并自我寡聚，导致caspase-1激活，pro-IL-1β和pro-IL-18成熟为生物活性细胞因子。这些生物活性细胞因子然后在炎症过程的起始和扩增中起关键作用。除了促进IL-1β和IL-18的蛋白水解激活外，炎症小体还通过caspase-1介导的细胞凋亡参与细胞死亡。在这篇综述中，我们描述了炎性小体的结构和功能，并概述了我们目前对炎性小体在气道炎症中的作用的了解。我们关注核苷酸结合结构域和富含亮氨酸的重复蛋白3（NLRP3）炎性小体，因为它是气道中表现出的最典型的亚型，并被认为在慢性气道疾病（例如哮喘）中起关键作用。

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