Inflammatory responses to metal oxide ceramic nanopowders

Abstract Ceramic orthopaedic implants are increasingly popular due to the need for robust total joint replacement implants that have a high success rate long-term and do not induce biological responses in patients. This study was designed to investigate the biological effects of ceramic nanopowders...

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Autores principales:	Shannon Jamieson, Amy Mawdesley, David Deehan, John Kirby, James Holland, Alison Tyson-Capper
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/984a342464d141d0bdb09117b3a5ba8e
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spelling	oai:doaj.org-article:984a342464d141d0bdb09117b3a5ba8e2021-12-02T15:53:10ZInflammatory responses to metal oxide ceramic nanopowders10.1038/s41598-021-89329-72045-2322https://doaj.org/article/984a342464d141d0bdb09117b3a5ba8e2021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-89329-7https://doaj.org/toc/2045-2322Abstract Ceramic orthopaedic implants are increasingly popular due to the need for robust total joint replacement implants that have a high success rate long-term and do not induce biological responses in patients. This study was designed to investigate the biological effects of ceramic nanopowders containing aluminium oxide or zirconium oxide to activate the human macrophage THP-1 cell line. In vitro investigation of pro-inflammatory gene expression and chemokine secretion was performed studied using RT-qPCR and ELISA, respectively. TLR4 inhibition, using a small-molecule inhibitor, was used to determine whether ceramic-mediated inflammation occurs in a similar manner to that of metals such as cobalt. THP-1 macrophages were primed with ceramics or LPS and then treated with ATP or ceramics, respectively, to determine whether these nanopowders are involved in the priming or activation of the NLRP3 inflammasome through IL-1β secretion. Cells treated with ceramics significantly increased pro-inflammatory gene expression and protein secretion which was attenuated through TLR4 blockade. Addition of ATP to cells following ceramic treatment significantly increased IL-1β secretion. Therefore, we identify the ability of ceramic metal oxides to cause a pro-inflammatory phenotype in THP-1 macrophages and propose the mechanism by which this occurs is primarily via the TLR4 pathway which contributes to inflammasome signalling.Shannon JamiesonAmy MawdesleyDavid DeehanJohn KirbyJames HollandAlison Tyson-CapperNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Shannon Jamieson Amy Mawdesley David Deehan John Kirby James Holland Alison Tyson-Capper Inflammatory responses to metal oxide ceramic nanopowders
description	Abstract Ceramic orthopaedic implants are increasingly popular due to the need for robust total joint replacement implants that have a high success rate long-term and do not induce biological responses in patients. This study was designed to investigate the biological effects of ceramic nanopowders containing aluminium oxide or zirconium oxide to activate the human macrophage THP-1 cell line. In vitro investigation of pro-inflammatory gene expression and chemokine secretion was performed studied using RT-qPCR and ELISA, respectively. TLR4 inhibition, using a small-molecule inhibitor, was used to determine whether ceramic-mediated inflammation occurs in a similar manner to that of metals such as cobalt. THP-1 macrophages were primed with ceramics or LPS and then treated with ATP or ceramics, respectively, to determine whether these nanopowders are involved in the priming or activation of the NLRP3 inflammasome through IL-1β secretion. Cells treated with ceramics significantly increased pro-inflammatory gene expression and protein secretion which was attenuated through TLR4 blockade. Addition of ATP to cells following ceramic treatment significantly increased IL-1β secretion. Therefore, we identify the ability of ceramic metal oxides to cause a pro-inflammatory phenotype in THP-1 macrophages and propose the mechanism by which this occurs is primarily via the TLR4 pathway which contributes to inflammasome signalling.
format	article
author	Shannon Jamieson Amy Mawdesley David Deehan John Kirby James Holland Alison Tyson-Capper
author_facet	Shannon Jamieson Amy Mawdesley David Deehan John Kirby James Holland Alison Tyson-Capper
author_sort	Shannon Jamieson
title	Inflammatory responses to metal oxide ceramic nanopowders
title_short	Inflammatory responses to metal oxide ceramic nanopowders
title_full	Inflammatory responses to metal oxide ceramic nanopowders
title_fullStr	Inflammatory responses to metal oxide ceramic nanopowders
title_full_unstemmed	Inflammatory responses to metal oxide ceramic nanopowders
title_sort	inflammatory responses to metal oxide ceramic nanopowders
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/984a342464d141d0bdb09117b3a5ba8e
work_keys_str_mv	AT shannonjamieson inflammatoryresponsestometaloxideceramicnanopowders AT amymawdesley inflammatoryresponsestometaloxideceramicnanopowders AT daviddeehan inflammatoryresponsestometaloxideceramicnanopowders AT johnkirby inflammatoryresponsestometaloxideceramicnanopowders AT jamesholland inflammatoryresponsestometaloxideceramicnanopowders AT alisontysoncapper inflammatoryresponsestometaloxideceramicnanopowders
_version_	1718385525014921216

Inflammatory responses to metal oxide ceramic nanopowders

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