Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, China.
Front Immunol. 2021 Jul 21;12:720049. doi: 10.3389/fimmu.2021.720049. eCollection 2021.
Cigarette smoke damages a wide range of immunological functions, including innate and adaptive immune responses. Emerging literature demonstrates that inflammasome constitutes an essential component in innate immune response. In this review, we focus on the cumulative mechanisms of inflammasome in cigarette smoke-related diseases and physiopathological disorders, and summarize potential therapeutic opportunities targeting inflammasome. This review suggests that inflammasomes (NLRP3, NLRP6, NLRP12 and AIM2) are involved in the pathogenesis of several cigarette smoke-related diseases (including COPD, ALI, atherosclerosis, kidney injury, bladder dysfunction, and oral leukoplakia) and physiopathological disorders (macrophage dysfunction, endothelial barrier dysfunction, podocyte injury, and ubiquitin-mediated proteasomal processing). MyD88/NF-κB, HMGB1, production of ROS, endoplasmic reticulum stress and mitochondrial dysfunction, and Ca influx are potentially involved in cigarette smoke induced-inflammasome activation. Strategies targeting ROS/NLRP3 inflammasome axis are most widely investigated and show potential therapeutic effects.
香烟烟雾会损害多种免疫功能，包括先天免疫和适应性免疫反应。新出现的文献表明，炎症小体是先天免疫反应的重要组成部分。在这篇综述中，我们重点关注炎症小体在与香烟烟雾相关的疾病和生理病理紊乱中的累积机制，并总结了针对炎症小体的潜在治疗机会。这篇综述表明，炎症小体（NLRP3、NLRP6、NLRP12 和 AIM2）参与了几种与香烟烟雾相关的疾病（包括 COPD、ALI、动脉粥样硬化、肾损伤、膀胱功能障碍和口腔白斑病）和生理病理紊乱（巨噬细胞功能障碍、内皮屏障功能障碍、足细胞损伤和泛素介导的蛋白酶体加工）的发病机制。MyD88/NF-κB、HMGB1、ROS 的产生、内质网应激和线粒体功能障碍以及 Ca2+内流可能参与了香烟烟雾诱导的炎症小体激活。针对 ROS/NLRP3 炎症小体轴的策略研究最多，显示出潜在的治疗效果。
