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Fig. 1 | Particle and Fibre Toxicology

Fig. 1

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

Fig. 1

A general schematic diagram describing the components, assembly, and biologic events linked to activation of the NLRP3 inflammasome. Exposure to asbestos, erionite, CS, or PM may prime and activate the NLRP3 inflammasome via multiple mechanisms and the mechanisms detailed in Fig. 2. These fibres and particles induce dose-related damage to the cell membrane at high concentrations, are phagocytized, and can rupture phagolysosomes (PL). These processes and iron-dependent reactions on the particle surface may result in the elaboration of ROS via many routes. Inflammasome-associated caspase-1 activation leads directly to the maturation and secretion of IL-1β and IL-18. Another important function of inflammasomes is the induction of caspase-1 dependent pyroptosis which is a form of cell death characterized by both apoptosis and necrosis. This results in release of IL-1β and IL-18 as well as other inflammatory mediators such as IL-1α and HMGB1. These chemokines and cytokines either directly or indirectly lead to acute and chronic inflammation, the latter resulting in various particle and fibre-associated lung and pleural diseases. Although IL-33 is sometimes released after pathogenic particle exposures, it is unclear whether or not it plays a critical role in IL-1β maturation or production

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