Nanoporous silica microparticle interaction with toll-like receptor agonists in macrophages

被引:22
作者
Cejudo-Guillen, M. [1 ,2 ]
Ramiro-Gutierrez, M. L. [3 ]
Labrador-Garrido, A. [1 ,2 ]
Diaz-Cuenca, A. [3 ]
Pozo, D. [1 ,2 ,4 ]
机构
[1] CABIMER Andalusian Ctr Mol Biol & Regenerat Med C, E-41092 Seville, Spain
[2] Univ Seville Med Sch, Dept Med Biochem Mol Biol & Immunol, E-41009 Seville, Spain
[3] CSIC Univ Seville, Mat Sci Inst Seville ICMS, E-41092 Seville, Spain
[4] BIONAND Andalusian Ctr Nanomed & Biotechnol, E-29590 Malaga, Spain
关键词
Nanoporous silica microparticles; Macrophage; Innate immunity; Toll-like receptor; MESOPOROUS SILICA; DRUG-DELIVERY; INNATE IMMUNITY; IN-VITRO; NANOPARTICLES; CELLS; BIOCOMPATIBILITY; PARTICLES; FUNCTIONALIZATION; CYTOTOXICITY;
D O I
10.1016/j.actbio.2012.07.026
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Nanoporous silica microparticles (NSiO2-MP) are considered to be potential drug delivery systems and scaffolding platforms in tissue engineering. However, few biocompatibility studies regarding NSiO2-MP interaction with the immune system have been reported. Toll-like receptors (TLR) are involved in host defence as well as autoimmune and inflammatory diseases. The results show that NSiO2-MP up to 100 mu g ml(-1) do not affect macrophage cell viability after 24 h cell culture. Moreover, NSiO2-MP do not compromise the cell viability of TLR-activated Raw 264.7 cells, for either cell surface TLR (TLR1/TLR2/TLR4/TLR6) or endocytic compartment TLR (TLR3/TLR7/TLR9). Furthermore, Raw 264.7 cells do not respond to NSiO2-MP exposure in terms of IL-6 or IL-10 secretion. NSiO2-MP co-treatment in the presence of TLR ligands does not impair or enhance the secretion of the pro-inflammatory cytokine IL-6 or the regulatory cytokine IL-10. Thus, NSiO2-MP do not affect macrophage polarization towards a pro-inflammatory or immunosuppressive status, representing added value in terms of biocompatibility compared with other SiO2-based micro- and nanoparticles. (C) 2012 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:4295 / 4303
页数:9
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