Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo
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...
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Karger Publishers
2021
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oai:doaj.org-article:71902c7dfc9b445eb4a81acd9fe93fe12021-11-04T14:40:31ZActivation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo1662-811X1662-812810.1159/000518953https://doaj.org/article/71902c7dfc9b445eb4a81acd9fe93fe12021-10-01T00:00:00Zhttps://www.karger.com/Article/FullText/518953https://doaj.org/toc/1662-811Xhttps://doaj.org/toc/1662-8128Beta-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.Kouji MaruyamaJin-Yan ChengHidee IshiiYu TakahashiVincent ZangiacomiTakatomo SatohTetsuji HosonoKen YamaguchiKarger Publishersarticlebeta-tricalcium phosphateinflammasomedendritic cellmacrophagethp-1 cellimmunomodulationMedicineRInternal medicineRC31-1245ENJournal of Innate Immunity, Pp 1-11 (2021) |
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DOAJ |
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EN |
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beta-tricalcium phosphate inflammasome dendritic cell macrophage thp-1 cell immunomodulation Medicine R Internal medicine RC31-1245 |
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beta-tricalcium phosphate inflammasome dendritic cell macrophage thp-1 cell immunomodulation Medicine R Internal medicine RC31-1245 Kouji Maruyama Jin-Yan Cheng Hidee Ishii Yu Takahashi Vincent Zangiacomi Takatomo Satoh Tetsuji Hosono Ken Yamaguchi Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo |
description |
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. |
format |
article |
author |
Kouji Maruyama Jin-Yan Cheng Hidee Ishii Yu Takahashi Vincent Zangiacomi Takatomo Satoh Tetsuji Hosono Ken Yamaguchi |
author_facet |
Kouji Maruyama Jin-Yan Cheng Hidee Ishii Yu Takahashi Vincent Zangiacomi Takatomo Satoh Tetsuji Hosono Ken Yamaguchi |
author_sort |
Kouji Maruyama |
title |
Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo |
title_short |
Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo |
title_full |
Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo |
title_fullStr |
Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo |
title_full_unstemmed |
Activation of NLRP3 Inflammasome Complexes by Beta-Tricalcium Phosphate Particles and Stimulation of Immune Cell Migration in vivo |
title_sort |
activation of nlrp3 inflammasome complexes by beta-tricalcium phosphate particles and stimulation of immune cell migration in vivo |
publisher |
Karger Publishers |
publishDate |
2021 |
url |
https://doaj.org/article/71902c7dfc9b445eb4a81acd9fe93fe1 |
work_keys_str_mv |
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