Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo
Autor: | Yu Takahashi, Ken Yamaguchi, Takatomo Satoh, Jin-Yan Cheng, Hidee Ishii, Kouji Maruyama, Tetsuji Hosono, Vincent Zangiacomi |
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Rok vydání: | 2021 |
Předmět: |
Calcium Phosphates
Inflammasomes dendritic cell Phagocytosis Interleukin-1beta macrophage immunomodulation Mice Immune system Cell Movement inflammasome In vivo NLR Family Pyrin Domain-Containing 3 Protein medicine Animals Immunology and Allergy Macrophage Internal medicine chemistry.chemical_classification Reactive oxygen species integumentary system Caspase 1 Interleukin Inflammasome Dendritic cell RC31-1245 Cell biology thp-1 cell chemistry Medicine Reactive Oxygen Species beta-tricalcium phosphate Research Article medicine.drug |
Zdroj: | Journal of Innate Immunity, Pp 1-11 (2021) J Innate Immun |
ISSN: | 1662-8128 1662-811X |
Popis: | Beta-tricalcium phosphate (β-TCP) serves as a bone substitute in clinical practice because it is resorbable, biocompatible, osteointegrative, and osteoconductive. Particles of β-TCP are also inflammatory mediators although the mechanism of this function has not been fully elucidated. Regardless, the ability of β-TCP to stimulate the immune system might be useful for immunomodulation. The present study aimed to determine the effects of β-TCP particles on NLR family pyrin domain containing 3 (NLRP3) inflammasome complexes. We found that β-TCP activates NLRP3 inflammasomes, and increases interleukin (IL)-1β production in primary cultured mouse dendritic cells (DCs) and macrophages, and human THP-1 cells in caspase-1 dependent manner. In THP-1 cells, β-TCP increased also IL-18 production, and NLRP3 inflammasome activation by β-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation. We also investigated the effects of β-TCP in wild-type and NLRP3-deficient mice in vivo. Immune cell migration around subcutaneously injected β-TCP particles was reduced in NLRP3-deficient mice. These findings suggest that the effects of β-TCP particles in vivo are at least partly mediated by NLRP3 inflammasome complexes. |
Databáze: | OpenAIRE |
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