Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, People's Republic of China; Department of Immunology, Anhui Provincial Key Laboratory of Infection and Immunity, Bengbu Medical College, Bengbu, Anhui 233030, People's Republic of China.
Department of Clinical Laboratory, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233030, People's Republic of China.
Trends Immunol. 2018 May;39(5):393-406. doi: 10.1016/j.it.2018.01.009. Epub 2018 Feb 13.
The assembly of the NLRP3 inflammasome can promote the release of IL-1β/IL-18 and initiate pyroptosis. Accordingly, the dysregulation of NLRP3 inflammasome activation is involved in a variety of human diseases, including gout, diabetes, and Alzheimer's disease. NLRP3 can sense a variety of structurally unrelated pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) to trigger inflammation, but the unifying mechanism of NLRP3 activation is still poorly understood. Increasing evidence suggests that intracellular ions, such as K, Ca, and Cl, have a significant role in NLRP3 inflammasome activation. Here, we review the current knowledge about the role of ionic fluxes in NLRP3 inflammasome activation and discuss how disturbances in intracellular ionic levels orchestrate different signaling events upstream of NLRP3.
NLRP3 炎性体的组装可以促进 IL-1β/IL-18 的释放，并引发细胞焦亡。因此，NLRP3 炎性体激活的失调与多种人类疾病有关，包括痛风、糖尿病和阿尔茨海默病。NLRP3 可以感知多种结构上无关的病原体相关分子模式（PAMPs）或危险相关分子模式（DAMPs）来引发炎症，但 NLRP3 激活的统一机制仍知之甚少。越来越多的证据表明，细胞内离子，如 K、Ca 和 Cl，在 NLRP3 炎性体激活中发挥重要作用。在这里，我们回顾了离子流在 NLRP3 炎性体激活中的作用的现有知识，并讨论了细胞内离子水平的紊乱如何协调 NLRP3 上游的不同信号事件。
