2. Academic Validation
  3. A tandem activation of NLRP3 inflammasome induced by copper oxide nanoparticles and dissolved copper ion in J774A.1 macrophage

A tandem activation of NLRP3 inflammasome induced by copper oxide nanoparticles and dissolved copper ion in J774A.1 macrophage

  • J Hazard Mater. 2021 Jun 5;411:125134. doi: 10.1016/j.jhazmat.2021.125134.
Xiaoqi Tao 1,  Xulin Wan 1,  Di Wu 2,  Erqun Song 2,  Yang Song 3
Affiliations

Affiliations

  • 1 Key Laboratory of Luminescence Analysis and Molecular Sensing, Ministry of Education, College of Food Science, Southwest University, Chongqing 400715, China.
  • 2 Key Laboratory of Luminescence Analysis and Molecular Sensing, Ministry of Education, College of Pharmaceutical Sciences, Southwest University, Chongqing 400715, China.
  • 3 Key Laboratory of Luminescence Analysis and Molecular Sensing, Ministry of Education, College of Pharmaceutical Sciences, Southwest University, Chongqing 400715, China; State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China. Electronic address: ysong@swu.edu.cn.
PMID: 33485222 DOI: 10.1016/j.jhazmat.2021.125134
Abstract

For the first time, we reported that CuONPs exposure induced interleukin (IL)-1β-mediated inflammation via NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome in J774A.1 macrophage. Mechanistically, CuONPs activated NLRP3 inflammasome is a two-fold process. Firstly, CuONPs challenge caused lysosomal damage, along with the release of Cathepsin B, which directly mediated the activation of NLRP3 inflammasomes. Interestingly, after the deposition in lysosomes, CuONPs may release copper ion due to the acidic environment of lysosomes. Consequently, the released copper ions significantly induced cellular oxidative stress and further mediated the activation of NLRP3 inflammasomes. Moreover, CuONPs exposure could prime J774A.1 macrophage to express pro-IL-1β through myeloid differentiation factor 88 (MyD88)-dependent Toll-like Receptor 4 (TLR4) signal pathway subsequently activating nuclear transcription factor kappa B (NF-κB).

Keywords

Cathepsin B; Copper oxide nanoparticles; Lysosomal damage; NLRP3 inflammasome; Reactive oxygen species.

Figures
Products
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-P1009
    ≥98.0%, Caspase 1/4 抑制剂
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