title: Activation of the NLRP3 inflammasome by proteins that signal for necroptosis.
abstract: Necroptosis-a form of programmed necrotic cell death-and its resulting release of damage-associated molecular patterns (DAMPs) are believed to participate in the triggering of inflammatory processes. To assess the relative contribution of this cell death mode to inflammation, we need to know what other cellular effects can be exerted by molecules shown to trigger necrotic death, and the extent to which those effects might themselves contribute to inflammation. Here, we describe the technical approaches that have been applied to assess the impact of the main signaling molecules known to mediate activation of necroptosis upon generation of inflammatory cytokines in LPS-treated mouse bone marrow-derived dendritic cells. The findings obtained by this assessment indicated that signaling molecules known to initiate necroptosis can also initiate activation of the NLRP3 inflammasome, thereby inducing inflammation independently of cell death by triggering the generation of proinflammatory cytokines such as IL-1β.
authors: Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel; Department of Biotechnology, College of Biomedical and Health Science, Konkuk University, Chung-Ju, Republic of Korea.
authors: Tae-Bong
authors: TB
authors: Kang
authors: Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
authors: Seung-Hoon
authors: SH
authors: Yang
authors: Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
authors: Beata
authors: B
authors: Toth
authors: Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
authors: Andrew
authors: A
authors: Kovalenko
authors: Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel. Electronic address: d.wallach@weizmann.ac.il.
authors: David
authors: D
authors: Wallach
mesh_terms: D000818:Animals; D002352:Carrier Proteins / Q000096:biosynthesis*; D053181:Caspase 8 / Q000096:biosynthesis; D016923:Cell Death / Q000235:genetics*; D003713:Dendritic Cells / Q000378:metabolism; D015971:Gene Expression Regulation, Enzymologic; D058847:Inflammasomes / Q000378:metabolism*; D007249:Inflammation / Q000139:chemically induced / Q000201:enzymology* / Q000235:genetics; D053583:Interleukin-1beta / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000633:toxicity; D051379:Mice; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D015398:Signal Transduction / Q000235:genetics
chemical_list: D002352:Carrier Proteins; C587672:IL1B protein, mouse; D058847:Inflammasomes; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C492716:Nlrp3 protein, mouse; D053181:Caspase 8
keywords: Caspase-8; DAMP; IL-1β; Inflammasome; Inflammation; MLKL; NLRP3; Necroptosis; Necrosis; RIPK3