|Nano-SiO2||Unit size||Cat. code||Docs||Qty||Price|
SiO2; Silicon Dioxid Nanoparticles
20 mg (2 x 10 mg)
NLRP3 Inflammasome Inducer - Silicon Dioxid Nanoparticles
SiO2 nanoparticles (Nano-SiO2) are single particles of silica dioxide, an inorganic metal oxide, with a diameter of less than 100 nm.
Several studies have demonstrated that Nano-SiO2 trigger the NLRP3 inflammasome-dependent induction of interleukin-1β (IL-1β) and IL-18 in vitro and in vivo [1,2].
InvivoGen also offers:
- Potent inducer of the NLRP3 inflammasome
- Nanoparticles with a diameter of <100 nm
- Each lot is functionally tested
Read our review on the NLRP3 inflammasome.
Download our Practical guide on Inflammasomes.
1. Nakayama M. et al., 2018. Macrophage recognition of crystals and nanoparticles. Front Immunol. 9:103.
2. He Y. et al., 2016. NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux. Nature. 530(7590):354-7.
IL-1β production in THP1-Null cells.
THP1-Null cells, primed with LPS (1 µg/ml for 3h), were stimulated with increasing concentrations of Nano-SiO2. After overnight incubation, IL-1β secretion was analyzed by adding 50 µl of supernatant from treated THP1-Null cells to HEK-Blue™ IL-1β cells. IL-1β-induced activation of NF-κB was assessed by measuring the levels of SEAP in the supernatant of HEK-Blue™ IL-1β cells using QUANTI-Blue™ Solution, and by reading the optical density (OD) at 630 nm.
Working concentration: 10-250 µg/ml
CAS number: 7631-86-9
Linear formula: SiO2
Molecular weight: 60.08 g/mol
- The biological activity has been validated using cellular assays.
- The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK-Blue™ TLR4 cells.
- 20 mg (2 x 10 mg) Nano-SiO2 (nanoparticles of silica dioxide)
Nano-SiO2 is shipped at room temperature.
Store at room temperature.Back to the top
The NLRP3 inflammasome is an intracellular multi-protein complex that plays a central role in innate immunity. It is activated by a two-step process. A first signal (‘priming’) is provided by pathogen-associated molecular patterns (PAMPs) or cytokines. It allows the transcriptional upregulation of key inflammasome actors and the post-translational modification of NLRP3 . The second signal (‘activation’) is provided by a wide array of stimuli including microbial toxins, endogenous molecules or crystalline substances. The current paradigm is that NLRP3 does not bind directly to these molecules. Rather it senses downstream cytosolic stress signals such as K+ efflux. This triggers inflammasome multimerization and pro-caspase-1 maturation. Proximity-induced autolytic activation of caspase-1 leads to the formation of gasdermin D (GSDMD) pores at the cell surface, allowing IL-1β/IL-18 and alarmin secretion, and ultimately, pyroptosis [1,2].
1. Swanson K.V. et al., 2019. The NLRP3 inflammasome: molecular activation and regulation to therapeutics. Nat. Rev. Immunol. 19:477.
2. Groslambert M. & Py B. 2018. Spotlight on the NLRP3 inflammasome pathway. J. Inflamm. Res. 11:359.