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10.1172/JCI94495 http://scihub22266oqcxt.onion/10.1172/JCI94495 C5663346!5663346!28990935     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest ä ; 127 (11): 4124-35 Nephropedia Template TP {{tp|p=28990935|t=ä. Caspase-11?mediated endothelial pyroptosis underlies endotoxemia-induced lung injury |pdf=|usr=}}{{28990935}} gab.com Text Caspase-11 mediated endothelial pyroptosis underlies endotoxemia-induced lung injury JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28990935 #FOAvip Acute lung injury is a leading cause of death in bacterial sepsis due to the wholesale destruction of the lung endothelial barrier, which results in protein-rich lung edema, influx of proinflammatory leukocytes, and intractable hypoxemia. Pyroptosis is a form of programmed lytic cell death that is triggered by inflammatory caspases, but little is known about its role in EC death and acute lung injury. Here, we show that systemic exposure to the bacterial endotoxin lipopolysaccharide (LPS) causes severe endothelial pyroptosis that is mediated by the inflammatory caspases, human caspases 4/5 in human ECs, or the murine homolog caspase-11 in mice in vivo. In caspase-11?deficient mice, BM transplantation with WT hematopoietic cells did not abrogate endotoxemia-induced acute lung injury, indicating a central role for nonhematopoietic caspase-11 in endotoxemia. Additionally, conditional deletion of caspase-11 in ECs reduced endotoxemia-induced lung edema, neutrophil accumulation, and death. These results establish the requisite role of endothelial pyroptosis in endotoxemic tissue injury and suggest that endothelial inflammatory caspases are an important therapeutic target for acute lung injury. Twit Text FOAVip Caspase-11 mediated endothelial pyroptosis underlies endotoxemia-induced lung injury ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28990935 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28990935 #FOAvip English Wikipedia <ref>{{Cite pmid|28990935}}</ref> Caspase-11?mediated endothelial pyroptosis underlies endotoxemia-induced lung injury #MMPMID28990935 Cheng KT; Xiong S; Ye Z; Hong Z; Di A; Tsang KM; Gao X; An S; Mittal M; Vogel SM; Miao EA; Rehman J; Malik AB J Clin Invest ä[]; 127 (11): 4124-35 PMID28990935show ga Acute lung injury is a leading cause of death in bacterial sepsis due to the wholesale destruction of the lung endothelial barrier, which results in protein-rich lung edema, influx of proinflammatory leukocytes, and intractable hypoxemia. Pyroptosis is a form of programmed lytic cell death that is triggered by inflammatory caspases, but little is known about its role in EC death and acute lung injury. Here, we show that systemic exposure to the bacterial endotoxin lipopolysaccharide (LPS) causes severe endothelial pyroptosis that is mediated by the inflammatory caspases, human caspases 4/5 in human ECs, or the murine homolog caspase-11 in mice in vivo. In caspase-11?deficient mice, BM transplantation with WT hematopoietic cells did not abrogate endotoxemia-induced acute lung injury, indicating a central role for nonhematopoietic caspase-11 in endotoxemia. Additionally, conditional deletion of caspase-11 in ECs reduced endotoxemia-induced lung edema, neutrophil accumulation, and death. These results establish the requisite role of endothelial pyroptosis in endotoxemic tissue injury and suggest that endothelial inflammatory caspases are an important therapeutic target for acute lung injury. äCaspase-11?mediated endothelial pyroptosis underlies endotoxemia-induc(epmc).pdf DeepDyve Pubget Overpricing