Basic calcium phosphate crystals induce monocyte/macrophage IL-1(beta) secretion through the NLRP3 inflammasome in vitro.

Details

Serval ID
serval:BIB_5814AFB917ED
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Basic calcium phosphate crystals induce monocyte/macrophage IL-1(beta) secretion through the NLRP3 inflammasome in vitro.
Journal
Journal of Immunology
Author(s)
Pazár B., Ea H.K., Narayan S., Kolly L., Bagnoud N., Chobaz V., Roger T., Lioté F., So A., Busso N.
ISSN
1550-6606 (Electronic)
ISSN-L
0022-1767
Publication state
Published
Issued date
2011
Volume
186
Number
4
Pages
2495-2502
Language
english
Abstract
Basic calcium phosphate (BCP) crystals are associated with severe osteoarthritis and acute periarticular inflammation. Three main forms of BCP crystals have been identified from pathological tissues: octacalcium phosphate, carbonate-substituted apatite, and hydroxyapatite. We investigated the proinflammatory effects of these BCP crystals in vitro with special regard to the involvement of the NLRP3-inflammasome in THP-1 cells, primary human monocytes and macrophages, and mouse bone marrow-derived macrophages (BMDM). THP-1 cells stimulated with BCP crystals produced IL-1β in a dose-dependent manner. Similarly, primary human cells and BMDM from wild-type mice also produced high concentrations of IL-1β after crystal stimulation. THP-1 cells transfected with short hairpin RNA against the components of the NLRP3 inflammasome and mouse BMDM from mice deficient for NLRP3, apoptosis-associated speck-like protein, or caspase-1 did not produce IL-1β after BCP crystal stimulation. BCP crystals induced macrophage apoptosis/necrosis as demonstrated by MTT and flow cytometric analysis. Collectively, these results demonstrate that BCP crystals induce IL-1β secretion through activating the NLRP3 inflammasome. Furthermore, we speculate that IL-1 blockade could be a novel strategy to inhibit BCP-induced inflammation in human disease.
Pubmed
Web of science
Open Access
Yes
Create date
06/04/2011 9:16
Last modification date
20/08/2019 14:11
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