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10.1038/s41419-018-0538-5 http://scihub22266oqcxt.onion/10.1038/s41419-018-0538-5 C5964241!5964241!29789550     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2018 ; 9 (6): ä Nephropedia Template TP {{tp|p=29789550|t=2018. Neutrophil extracellular traps promote macrophage pyroptosis in sepsis |pdf=|usr=}}{{29789550}} gab.com Text Neutrophil extracellular traps promote macrophage pyroptosis in sepsis JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29789550 #FOAvip In response to infection, polymorphonuclear neutrophils (PMN) are recruited in the infectious sites, and employ three major strategies to fight against the microbes including phagocytosis, degranulation, and neutrophil extracellular traps (NETs). NETs are a meshwork of chromatin fibers mixed with granule-derived antimicrobial peptides and enzymes, which trap and kill the bacteria extracellularly. In this study, by using a mouse sepsis model, we identified a novel mechanism by which NETs induce macrophage (M?) pyroptosis, a caspase-1-dependent regulated cell death. We show that NET-derived HMGB1, acting through RAGE and dynamin-dependent signaling, triggers an intra-M? cascade of molecular events including cathepsin B (CatB) release from the ruptured lysosomes, followed by pyroptosome formation and caspase-1 activation, and subsequent M? pyroptosis. The study further demonstrates that M? pyroptosis augments inflammatory responses following sepsis. These findings shed light on the proinflammatory role of NETs in mediating PMN?M? interaction, which therefore influences the progress of inflammation following infection. Twit Text FOAVip Neutrophil extracellular traps promote macrophage pyroptosis in sepsis ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=29789550 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29789550 #FOAvip English Wikipedia <ref>{{Cite pmid|29789550}}</ref> Neutrophil extracellular traps promote macrophage pyroptosis in sepsis #MMPMID29789550 Chen L; Zhao Y; Lai D; Zhang P; Yang Y; Li Y; Fei K; Jiang G; Fan J Cell Death Dis 2018[Jun]; 9 (6): ä PMID29789550show ga In response to infection, polymorphonuclear neutrophils (PMN) are recruited in the infectious sites, and employ three major strategies to fight against the microbes including phagocytosis, degranulation, and neutrophil extracellular traps (NETs). NETs are a meshwork of chromatin fibers mixed with granule-derived antimicrobial peptides and enzymes, which trap and kill the bacteria extracellularly. In this study, by using a mouse sepsis model, we identified a novel mechanism by which NETs induce macrophage (M?) pyroptosis, a caspase-1-dependent regulated cell death. We show that NET-derived HMGB1, acting through RAGE and dynamin-dependent signaling, triggers an intra-M? cascade of molecular events including cathepsin B (CatB) release from the ruptured lysosomes, followed by pyroptosome formation and caspase-1 activation, and subsequent M? pyroptosis. The study further demonstrates that M? pyroptosis augments inflammatory responses following sepsis. These findings shed light on the proinflammatory role of NETs in mediating PMN?M? interaction, which therefore influences the progress of inflammation following infection. äNeutrophil extracellular traps promote macrophage pyroptosis in sepsis(epmc).pdf DeepDyve Pubget Overpricing