Activation of NLRP3 inflammasome in hepatocytes after exposure to cobalt nanoparticles: The role of oxidative stress

Induction of Cytokines by Nucleic Acid Nanoparticles (NANPs) Depends on the Type of Delivery Carrier

“…Our results, therefore, suggest that NANPs delivered by cationic dendrimers are perceived by immune cells as danger signals, hence the induction of IL-1α, IL-6, and IL-8 [ 24 ]. Cationic nanoparticles activate the inflammasome, thereby contributing to the secretion of mature IL-1β, expression of which is induced by other stimuli [ 53 , 54 , 55 ]. The induction of IL-1β observed in supernatants from cells treated with NANP–dendrimer complexes is consistent with this knowledge; the data suggest that NANPs induce IL-1β expression whereas cationic dendrimers activate the inflammasome to produce mature IL-1β proteins.…”

Understanding the cellular interactome of non-alcoholic fatty liver disease

“…They release damage-associated molecular patterns (DAMPs), such as DNA fragments, histones, ATP, uric acid and cholesterol crystals, that act as stress signals to activate DAMP receptors, such as TLRs, P2X and P2Y purinoreceptors and C-type lectin domain (CLEC)12A, which activate innate immunity and inflammation, and often exacerbate tissue injury. 34 They also secrete inflammatory and fibrogenic cytokines either directly, such as interleukin (IL)-1b and IL-18, 35,36 or via extracellular vesicles containing C-X-C motif chemokine ligand (CXCL)10, a ligand for C-X-C motif chemokine receptor (CXCR)3, and mitochondrial DNA, a key TLR9 ligand. 37 Hedgehog pathway activation is triggered by injured, ballooned and/or TAZ-expressing hepatocytes in NASH via the release of sonic hedgehog or Indian hedgehog.…”

The importance of the IL‐1 family of cytokines in nanoimmunosafety and nanotoxicology

“…Prof. Jürg Tschopp's group reported that nano‐TiO 2 and nano‐SiO 2 , but not nano‐ZnO, induced NLRP3 inflammasome activation and IL‐1β secretion, as well as IL‐1α secretion (Yazdi et al, 2010), suggesting that inflammasome activation is likely dependent on the chemical compound. To date, three models by which ENMs modulate inflammasome activation have been proposed and are shown in Figure 1: (a) stimuli that open ion channels (K + efflux or Ca 2+ influx via ion channels or ATP influx via ATP channels; Baron et al, 2015; Yang et al, 2012; Yaron et al, 2015), (b) lysosomal rupture and release of cathepsins (Ji et al, 2012; Lunov et al, 2011), and (c) ROS generation (Dostert et al, 2008; Feng et al, 2020). However, the exact molecular mechanisms by which ENMs stimulate this action remain unclear (Wang et al, 2020).…”