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The Effects of Silica Nanoparticles in Macrophage Cells
Immune Network ; : 296-300, 2012.
Artículo en Inglés | WPRIM | ID: wpr-20061
ABSTRACT
Silica nanoparticles, which are applicable in many industrial fields, have been reported to induce cellular changes such as cytotoxicity in various cells and fibrosis in lungs. Because the immune system is the primary targeting organ reacting to internalized exogenous nanoparticles, we tried to figure out the immunostimulatory effect of silica nanoparticles in macrophages using differently sized silica nanoparticles. Using U937 cells we assessed cytotoxicity by CCK-8 assay, ROS generation by CM-H2DCFDA, intracellular Ca++ levels by staining with Fluo4-AM and IL-8 production by ELISA. At non-toxic concentration, the intracellular Ca++ level has increased immediately after exposure to 15 nm particles, not to larger particles. ROS generation was detected significantly in response to 15 nm particles. However, all three different sizes of silica nanoparticles induced IL-8 production. 15 nm silica nanoparticles are more stimulatory than larger particles in cytotoxicity, intracellular Ca++ increase and ROS generation. But IL-8 production was induced to same levels with 50 or 100 nm particles. Therefore, IL-8 production induced by silica nanoparticles may be dependent on other mechanisms rather than intracellular Ca++ increase and ROS generation.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Sincalida / Fibrosis / Ensayo de Inmunoadsorción Enzimática / Interleucina-8 / Dióxido de Silicio / Células U937 / Nanopartículas / Sistema Inmunológico / Pulmón / Macrófagos Idioma: Inglés Revista: Immune Network Año: 2012 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Sincalida / Fibrosis / Ensayo de Inmunoadsorción Enzimática / Interleucina-8 / Dióxido de Silicio / Células U937 / Nanopartículas / Sistema Inmunológico / Pulmón / Macrófagos Idioma: Inglés Revista: Immune Network Año: 2012 Tipo del documento: Artículo