Document Type
Article
Publication Date
2016
College/Unit
School of Medicine
Department/Program/Center
Orthopaedics
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.
Digital Commons Citation
Armstead, Andrea L. and Li, Bingyun, "In vitro inflammatory effects of hard metal (WC-Co) nanoparticle exposure" (2016). Faculty & Staff Scholarship. 907.
https://researchrepository.wvu.edu/faculty_publications/907
Source Citation
Armstead, A. L., & Li, B. (2016). In vitro inflammatory effects of hard metal (WC-Co) nanoparticle exposure. International Journal of Nanomedicine, 11.
Comments
The article is supported by the WVU Libraries' Open Access Author Fund.