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Fig. 2 | Particle and Fibre Toxicology

Fig. 2

From: The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases

Fig. 2

General mechanisms of inflammasome activation by pathogenic particles and fibres. Note that the complex cascades of specific proteins in these pathways are not presented. The numbers refer to individual pathways that include: 1) modifications in intracellular levels and export of K+ and Ca++; 2) formation and release of ROS both intracellularly and extracellularly that destabilize phagolysosomes, activate caspase-1; and 3) phagolysosomal disruption and increases in intracellular H+ (reviewed in [156, 157]). In addition to these classical pathways observed with diverse agents, studies with pathogenic particles and fibres show inflammasome priming or activation by: 4) release of ATP, ADP, and increases in purigenic receptor signaling; 5) elaboration of ROS by a multiplicity of pathways including generation mitochondrial oxidants/antioxidant enzymes and oxidation of mitochondrial DNA; 6) dose-dependent particle uptake; 7) Trx-1 oxidation and TXN1P disassociation; and 8) increases in cell volume via particle uptake, aquaporin channels (Rabolli et al., Part Fibre Toxicol, in press) and/or modulation of connexin/pannexin gap junctions that also are cytoskeletal organization proteins linked to both inflammation and immune regulation

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