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Comparison of non-crystalline silica nanoparticles in IL-1β release from macrophages

TitoloComparison of non-crystalline silica nanoparticles in IL-1β release from macrophages
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2012
AutoriSandberg, W.J., Låg M., Holme J.A., Friede B., Gualtieri Maurizio, Kruszewski M., Schwarze P.E., Skuland T., and Refsnes M.
RivistaParticle and Fibre Toxicology
Volume9
ISSN17438977
Parole chiaveacidification, Alveolar, animal cell, Animals, article, Bacteria (microorganisms), Biological Transport, caspase inhibitor, cathepsin B, Cell Line, Cells, controlled study, cryopyrin, Cultured, cytokine release, endosome, enzyme activity, gene silencing, immune response, Inbred WKY, Inflammasomes, interleukin 1beta, Interleukin-1beta, Lipopolysaccharides, lung alveolus macrophage, macrophage activation, macrophage function, Macrophages, male, Mice, Molecular Conformation, mouse, NALP3 receptor, nanoparticle, Nanoparticles, non crystalline silica nanoparticle, nonhuman, particle size, phagocytosis, Phagosomes, priority journal, rat, Rats, Rattus, Receptor, RNA, Silicon Dioxide, Surface properties, surface property, Transformed, unclassified drug
Abstract

Background: Respirable crystalline silica (silicon dioxide; SiO2, quartz) particles are known to induce chronic inflammation and lung disease upon long-term inhalation, whereas non-crystalline (amorphous) SiO2 particles in the submicrometre range are regarded as less harmful. Several reports have demonstrated that crystalline, but also non-crystalline silica particles induce IL-1β release from macrophages via the NALP3-inflammasome complex (caspase-1, ASC and NALP3) in the presence of lipopolysaccharide (LPS) from bacteria. Our aim was to study the potential of different non-crystalline SiO2 particles from the nano- to submicro-sized range to activate IL-1β responses in LPS-primed RAW264.7 macrophages and primary rat lung macrophages. The role of the NALP3-inflammasome and up-stream mechanisms was further explored in RAW264.7 cells.Results: In the present study, we have shown that 6 h exposure to non-crystalline SiO2 particles in nano- (SiNPs, 5-20 nm, 50 nm) and submicro-sizes induced strong IL-1β responses in LPS-primed mouse macrophages (RAW264.7) and primary rat lung macrophages. The primary lung macrophages were more sensitive to Si-exposure than the RAW-macrophages, and responded more strongly. In the lung macrophages, crystalline silica (MinUsil 5) induced IL-1β release more potently than the non-crystalline Si50 and Si500, when adjusted to surface area. This difference was much less pronounced versus fumed SiNPs. The caspase-1 inhibitor zYVAD and RNA silencing of the NALP3 receptor reduced the particle-induced IL-1β release in the RAW264.7 macrophages. Furthermore, inhibitors of phagocytosis, endosomal acidification, and cathepsin B activity reduced the IL-1β responses to the different particles to a similar extent.Conclusions: In conclusion, non-crystalline silica particles in the nano- and submicro-size ranges seemed to induce IL-1β release from LPS-primed RAW264.7 macrophages via similar mechanisms as crystalline silica, involving particle uptake, phagosomal leakage and activation of the NALP3 inflammasome. Notably, rat primary lung macrophages were more sensitive with respect to silica-induced IL-1β release. The differential response patterns obtained suggest that silica-induced IL-1β responses not only depend on the particle surface area, but on factors and/or mechanisms such as particle reactivity or particle uptake. These findings may suggest that bacterial infection via LPS may augment acute inflammatory effects of non-crystalline as well as crystalline silica particles. © 2012 Sandberg et al.; licensee BioMed Central Ltd.

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URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84864808636&doi=10.1186%2f1743-8977-9-32&partnerID=40&md5=0a9714470561c3ec6ef4e1385dcd9054
DOI10.1186/1743-8977-9-32
Citation KeySandberg2012