In vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure
Andrea L Armstead,1,2 Bingyun Li1–3 1Department of Orthopaedics, School of Medicine, 2School of Pharmacy, West Virginia University, 3Mary Babb Randolph Cancer Center, Morgantown, WV, USA Abstract: Identifying the toxicity of nanoparticles (NPs) is an important area of research as the&...
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Dove Medical Press
2016
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oai:doaj.org-article:99d9253b708e4842bec3f6ff8d1cc1712021-12-02T04:05:36ZIn vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure1178-2013https://doaj.org/article/99d9253b708e4842bec3f6ff8d1cc1712016-11-01T00:00:00Zhttps://www.dovepress.com/in-vitro-inflammatory-effects-of-hard-metal-wcndashco-nanoparticle-exp-peer-reviewed-article-IJNhttps://doaj.org/toc/1178-2013Andrea L Armstead,1,2 Bingyun Li1–3 1Department of Orthopaedics, School of Medicine, 2School of Pharmacy, West Virginia University, 3Mary Babb Randolph Cancer Center, Morgantown, WV, USA Abstract: Identifying the toxicity of nanoparticles (NPs) is an important area of research as the number of nanomaterial-based consumer and industrial products continually rises. In addition, the potential inflammatory effects resulting from pulmonary NP exposure are emerging as an important aspect of nanotoxicity. In this study, the toxicity and inflammatory state resulting from tungsten carbide–cobalt (WC–Co) NP exposure in macrophages and a coculture (CC) of lung epithelial cells (BEAS-2B) and macrophages (THP-1) at a 3:1 ratio were examined. It was found that the toxicity of nano-WC–Co was cell dependent; significantly less toxicity was observed in THP-1 cells compared to BEAS-2B cells. It was demonstrated that nano-WC–Co caused reduced toxicity in the CC model compared to lung epithelial cell monoculture, which suggested that macrophages may play a protective role against nano-WC–Co-mediated toxicity in CCs. Nano-WC–Co exposure in macrophages resulted in increased levels of interleukin (IL)-1β and IL-12 secretion and decreased levels of tumor necrosis factor alpha (TNFα). In addition, the polarizing effects of nano-WC–Co exposure toward the M1 (pro-inflammatory) and M2 (anti-inflammatory) macrophage phenotypes were investigated. The results of this study indicated that nano-WC–Co exposure stimulated the M1 phenotype, marked by high expression of CD40 M1 macrophage surface markers. Keywords: nanoparticle, nanotoxicity, inflammation, macrophage, lung disease Armstead ALLi BDove Medical Pressarticlenanoparticlenanotoxicityinflammationmacrophagelung diseaseMedicine (General)R5-920ENInternational Journal of Nanomedicine, Vol Volume 11, Pp 6195-6206 (2016) |
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DOAJ |
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EN |
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nanoparticle nanotoxicity inflammation macrophage lung disease Medicine (General) R5-920 |
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nanoparticle nanotoxicity inflammation macrophage lung disease Medicine (General) R5-920 Armstead AL Li B In vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure |
| description |
Andrea L Armstead,1,2 Bingyun Li1–3 1Department of Orthopaedics, School of Medicine, 2School of Pharmacy, West Virginia University, 3Mary Babb Randolph Cancer Center, Morgantown, WV, USA Abstract: Identifying the toxicity of nanoparticles (NPs) is an important area of research as the number of nanomaterial-based consumer and industrial products continually rises. In addition, the potential inflammatory effects resulting from pulmonary NP exposure are emerging as an important aspect of nanotoxicity. In this study, the toxicity and inflammatory state resulting from tungsten carbide–cobalt (WC–Co) NP exposure in macrophages and a coculture (CC) of lung epithelial cells (BEAS-2B) and macrophages (THP-1) at a 3:1 ratio were examined. It was found that the toxicity of nano-WC–Co was cell dependent; significantly less toxicity was observed in THP-1 cells compared to BEAS-2B cells. It was demonstrated that nano-WC–Co caused reduced toxicity in the CC model compared to lung epithelial cell monoculture, which suggested that macrophages may play a protective role against nano-WC–Co-mediated toxicity in CCs. Nano-WC–Co exposure in macrophages resulted in increased levels of interleukin (IL)-1β and IL-12 secretion and decreased levels of tumor necrosis factor alpha (TNFα). In addition, the polarizing effects of nano-WC–Co exposure toward the M1 (pro-inflammatory) and M2 (anti-inflammatory) macrophage phenotypes were investigated. The results of this study indicated that nano-WC–Co exposure stimulated the M1 phenotype, marked by high expression of CD40 M1 macrophage surface markers. Keywords: nanoparticle, nanotoxicity, inflammation, macrophage, lung disease |
| format |
article |
| author |
Armstead AL Li B |
| author_facet |
Armstead AL Li B |
| author_sort |
Armstead AL |
| title |
In vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure |
| title_short |
In vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure |
| title_full |
In vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure |
| title_fullStr |
In vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure |
| title_full_unstemmed |
In vitro inflammatory effects of hard metal (WC–Co) nanoparticle exposure |
| title_sort |
in vitro inflammatory effects of hard metal (wc–co) nanoparticle exposure |
| publisher |
Dove Medical Press |
| publishDate |
2016 |
| url |
https://doaj.org/article/99d9253b708e4842bec3f6ff8d1cc171 |
| work_keys_str_mv |
AT armsteadal invitroinflammatoryeffectsofhardmetalwcndashconanoparticleexposure AT lib invitroinflammatoryeffectsofhardmetalwcndashconanoparticleexposure |
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