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Activation of nucleotide-binding domain-like receptor containing protein 3 inflammasome in dendritic cells and macrophages by Streptococcus sanguinis
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open access |
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This is the peer reviewed version of the following article: [Activation of nucleotide-binding domain-like receptor containing protein 3 inflammasome in dendritic cells and macrophages by Streptococcus sanguinis.], which has been published in final form at [http://doi.org/10.1111/cmi.12663]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
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Abstract
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Streptococcus sanguinis is frequently isolated from the blood of patients with infective endocarditis and contributes to the pathology of this disease through induction of interleukin (IL)-1β responsible for the development of the disease. However, the mechanism of IL-1β induction remains unknown. In this study, S. sanguinis activated a murine dendritic cell (DC) to induce IL-1β and this activity was attenuated by silencing the mRNAs of nucleotide-binding domain-like receptor containing protein 3 (NLRP3) and caspase-1. S. sanguinis induced IL-1β production in murine bone marrow-derived macrophage (BMM), but this activity was significantly reduced in BMMs from NLRP3-, apoptosis-associated speck-like protein containing a caspase-recruitment domain-, and caspase-1-deficient mice. DC phagocytosed S. sanguinis cells, followed by the release of adenosine triphosphate (ATP). The ATP-degradating enzyme attenuated the release of ATP and IL-1β. The inhibitors for ATP receptor reduced IL-1β release in DC. These results strongly suggest that S. sanguinis has the activity to induce IL-1β through the NLRP3 inflammasome in macrophage and DC and interaction of purinergic receptors with ATP released is involved in expression of the activity.
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Wiley-Blackwell
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journal article |
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AM |
Identifier |
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http://hdl.handle.net/2115/68426
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isVersionOf
DOI
https://doi.org/10.1111/cmi.12663
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PMID
27601185
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Journal |
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PISSN
1462-5814
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EISSN
1462-5822
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Cellular Microbiology
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Volume Number19
Issue Number3
Page Starte12663
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2023-08-19 |