The Nalp3 inflammasome is essential for the development of silicosis

By S. Cassel, S. Eisenbarth, S. Iyer, J. Sadler, O. Colegio, L. Tephly, A. Carter, P. Rothman, R. Flavell, F. Sutterwala. Proceedings of the National Academy of Sciences of the United States of America, 2008

915 citations recorded by the source corpus.

Subfields: Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/3fdd997f241e00bfc5f5bccdb48ec99048949b0e

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In Molecular Biology

1. J. Tschopp
2. G. Núñez
3. T. Kanneganti
4. M. Lamkanfi
5. V. Dixit
6. E. Latz
7. Fabio Martinon
8. Annick Mayor

In Pulmonary and Respiratory Medicine

1. TA Wynn
2. M. Wilson
3. T. Ramalingam

Citations in the corpus

• iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns (2012, background): “The NALP3 inflammasome activates caspase-1 that cleaves IL-1β precursor to active IL-1β that is rapidly secreted (Cassel et al., 2008; Dostert et al., 2008).”
• Macrophages and Tissue Injury: Agents of Defense or Destruction? (2011, background): “N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript Table 1 Mediators released by classically (M1) and alternatively (M2) activated macrophages implicated in liver and lung injury and ”
• Inflammasomes in health and disease (2012, background): “Examples of exogenous activators are silica and asbestos, whose endocytosis by pulmonary macrophages results in NLRP3 inflammasome activation involving ROS and lysosome destabilization, leading in turn to silicosis and asbestosis, respectivel”
• NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis. (2018, background): “For example, inhalation of asbestos, silica, and other crystals, which were shown to activate the NLRP3 inflammasome, lead to the development of progressive pulmonary fibrosis.(111,130,131) Even everyday inhaled particulate matter because of air pollution causes NLRP3 activation(132) and most likely”
• Glyburide inhibits the Cryopyrin/Nalp3 inflammasome (2009, background): “These results may have significant therapeutic ramifications for the treatment of gouty arthritis, silicosis, and Alzheimer’s, in which excessive Cryopyrin-dependent IL-1 production was proposed as a major cause of pathology (Cassel et al., 2008; Dostert et al., 2008; Halle et al., 2008; Hornung et”
• The inflammasomes: guardians of the body. (2009, background): “It is significant to note that pulmonary inflammation is greatly reduced in NALP3-deficient mice after in vivo inhalation of asbestos or silica (127, 128).”
• Sterile inflammation: sensing and reacting to damage (2010, background): “Consistently, in mouse models of sterile injury, such as gout, asbestosis and silicosis, NLRP3-deficient mice exhibited decreased inflammation with reduced levels of tissue infiltration by neutrophils or macrophage”
• The Inflammasome: A Caspase-1 Activation Platform Regulating Immune Responses and Disease Pathogenesis (2009, background): “Another set of stimuli that induce activation of the NLRP3 inflammasome is represented by silica and asbesto”
• The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation (2016, background): “…activation is observed in susceptible rat strains (Cirelli et al., 2014) and is a major determinant of parasite control in infected macrophages (Cavailles et al., 2014), although activation of NLRP1b through this parasite does not result in detectable levels of an NLRP1b cleavage product…”
• Integrating mechanisms of pulmonary fibrosis (2011, background): “…acid (induced by bleomycin), asbestos, and silica are detected by the Nalp3 inflammasome in macrophages, leading to IL-1R1/MyD88 signaling that is critical in the pathogenesis of particulate matter and bleomycin-driven fibrosis (Gasse et al., 2007, 2009; Cassel et al., 2008; Dostert et al., 2008).”
• The sterile inflammatory response (2010, background): “Do these same mechanisms operate in animals during a sterile inflammatory response? There is limited data that sterile inflammation stimulated by MSU (23), silica (89), cholesterol (Duewell et al.”