Figure 2.

The NLRP3 inflammasome in lung inflammation and injury. Evidence from patients with lung diseases and experimental animal models suggests that a number of inhaled triggers can cause NLRP3 inflammasome activation in the lung, including cigarette smoke, asbestos, silica, bleomycin, and IAV. Inhaled silica crystals or asbestos fibers can induce NLRP3 activation directly via lysosomal damage and ROS production after phagocytosis by alveolar macrophages. The NLRP3 inflammasome can also be activated indirectly in the lung after the release of danger signals from dying or injured cells (eg, eATP and uric acid crystals). Activation of the NLRP3 inflammasome drives the production of IL-1β and IL-18 cytokines, causing the infiltration of additional immune cells and lymphocytes that sustain the inflammatory response potentially leading to chronic lung injury and pulmonary fibrosis.