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Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
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Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
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Journal Article
Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
2008
Overview
The inhalation of airborne pollutants, such as asbestos or silica, is linked to inflammation of the lung, fibrosis, and lung cancer. How the presence of pathogenic dust is recognized and how chronic inflammatory diseases are triggered are poorly understood. Here, we show that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin-1β secretion. Inflammasome activation is triggered by reactive oxygen species, which are generated by a NADPH oxidase upon particle phagocytosis. (NADPH is the reduced form of nicotinamide adenine dinucleotide phosphate.) In a model of asbestos inhalation, Nalp3
–/–
mice showed diminished recruitment of inflammatory cells to the lungs, paralleled by lower cytokine production. Our findings implicate the Nalp3 inflammasome in particulate matter–related pulmonary diseases and support its role as a major proinflammatory “danger” receptor.
Publisher
American Association for the Advancement of Science,The American Association for the Advancement of Science
Subject
/ Animals
/ Asbestos
/ Biological and medical sciences
/ Carrier Proteins - physiology
/ Dust
/ fibrosis
/ Fundamental and applied biological sciences. Psychology
/ Humans
/ Immunity
/ Inflammation Mediators - physiology
/ Interleukin-1beta - metabolism
/ lungs
/ Mice
/ Molecular and cellular biology
/ NAD(P)H oxidase (H2O2-forming)
/ NLR Family, Pyrin Domain-Containing 3 Protein
/ Silica
