Inflammasome Activity in Non-Microbial Lung Inflammation.
Inflammasome Activity in Non-Microbial Lung Inflammation.
复制标题
DOI：
10.7178/jeit.20
复制
发表时间：
2014-09
期刊：
影响因子：
--
通讯作者：
J. Ather;Rebecca A. Martin;K. Ckless;M. Poynter
中科院分区：
文献类型：
--
作者：
J. Ather;Rebecca A. Martin;K. Ckless;M. Poynter
对白细胞介素-1 （IL-1）家族细胞因子在炎症性疾病中的理解已经迅速发展，部分原因是炎症小体的发现和表征，炎症小体是多亚基细胞内蛋白支架，主要能够识别无数的细胞刺激，导致caspase-1的激活和IL-1β和IL-18的加工。研究继续阐明炎症小体在微生物和环境因素诱导的免疫反应中的作用。本文综述了目前对肺内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，以及暴露于创伤和预先存在的炎症条件，如代谢综合征。这些无菌炎症状态下的炎性小体活性有助于哮喘、慢性阻塞性疾病、急性肺损伤、呼吸机诱导的肺损伤、肺纤维化和肺癌等疾病的发生。
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.