非微生物性肺部炎症中的炎性小体活性
Inflammasome Activity in Non-Microbial Lung Inflammation.
作者信息
Ather Jennifer L, Martin Rebecca A, Ckless Karina, Poynter Matthew E
机构信息
Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, USA.
Chemistry Department, State University of New York at Plattsburgh, Plattsburgh, USA.
出版信息
J Environ Immunol Toxicol. 2014 Sep 20;1(3):108-117.
The understanding of interleukin-1 (IL-1) family cytokines in inflammatory disease has rapidly developed, due in part to the discovery and characterization of inflammasomes, which are multi-subunit intracellular protein scaffolds principally enabling recognition of a myriad of cellular stimuli, leading to the activation of caspase-1 and the processing of IL-1β and IL-18. Studies continue to elucidate the role of inflammasomes in immune responses induced by both microbes and environmental factors. This review focuses on the current understanding of inflammasome activity in the lung, with particular focus on the non-microbial instigators of inflammasome activation, including inhaled antigens, oxidants, cigarette smoke, diesel exhaust particles, mineral fibers, and engineered nanomaterials, as well as exposure to trauma and pre-existing inflammatory conditions such as metabolic syndrome. Inflammasome activity in these sterile inflammatory states contribute to diseases including asthma, chronic obstructive disease, acute lung injury, ventilator-induced lung injury, pulmonary fibrosis, and lung cancer.
对白细胞介素-1（IL-1）家族细胞因子在炎症性疾病中的认识迅速发展，部分原因是炎性小体的发现和特性鉴定，炎性小体是多亚基细胞内蛋白质支架，主要能够识别多种细胞刺激，导致半胱天冬酶-1激活以及IL-1β和IL-18的加工。研究不断阐明炎性小体在微生物和环境因素诱导的免疫反应中的作用。本综述重点关注目前对肺部炎性小体活性的理解，特别关注炎性小体激活的非微生物诱因，包括吸入抗原、氧化剂、香烟烟雾、柴油废气颗粒、矿物纤维和工程纳米材料，以及遭受创伤和存在如代谢综合征等先前存在的炎症状况。这些无菌炎症状态下的炎性小体活性会导致包括哮喘、慢性阻塞性疾病、急性肺损伤、呼吸机诱导的肺损伤、肺纤维化和肺癌在内的疾病。
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