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10.1097/SHK.0000000000000520 http://scihub22266oqcxt.onion/10.1097/SHK.0000000000000520 C4792770!4792770!26618986     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Shock 2016 ; 45 (4): 393-403 Nephropedia Template TP {{tp|p=26618986|t=2016. A PPAR? agonist enhances bacterial clearance through neutrophil extracellular trap formation and improves survival in sepsis |pdf=|usr=}}{{26618986}} gab.com Text A PPAR agonist enhances bacterial clearance through neutrophil extracellular trap formation and improves survival in sepsis JO: Shock http://www.kidney.de/pget.php?&tw=1&pmid=26618986 #FOAvip Dysregulation of the inflammatory response against infection contributes to mortality in sepsis. Inflammation provides critical host defense, but it can cause tissue damage, multiple organ failure and death. Because the nuclear transcription factor peroxisome proliferator-activated receptor ? (PPAR?) exhibits therapeutic potential, we characterized the role of PPAR? in sepsis. We analyzed severity of clinical signs, survival rates, cytokine production, leukocyte influx, and bacterial clearance in a cecal ligation and puncture (CLP) model of sepsis in Swiss mice. The PPAR? agonist rosiglitazone treatment improved clinical status and mortality, while increasing IL-10 production and decreasing TNF-? and IL-6 levels, and peritoneal neutrophil accumulation 24 h after CLP. We noted increased bacterial killing in rosiglitazone treated mice, correlated with increased generation of reactive oxygen species. Polymorphonuclear leukocytes (PMN) incubated with LPS or E. coli and rosiglitazone increased peritoneal neutrophil extracellular trap (NET)-mediated bacterial killing, an effect reversed by the PPAR? antagonist (GW 9662) treatment. Rosiglitazone also enhanced the release of histones by PMN, a surrogate marker of NET formation, effect abolished by GW 9662. Rosiglitazone modulated the inflammatory response and increased bacterial clearance through PPAR? activation and NET formation, combining immunomodulatory and host-dependent anti-bacterial effects and, therefore, warrants further study as a potential therapeutic agent in sepsis. Twit Text FOAVip A PPAR agonist enhances bacterial clearance through neutrophil extracellular trap formation and improves survival in sepsis ????Shock http://www.kidney.de/pget.php?&tw=1&pmid=26618986 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26618986 #FOAvip English Wikipedia <ref>{{Cite pmid|26618986}}</ref> A PPAR? agonist enhances bacterial clearance through neutrophil extracellular trap formation and improves survival in sepsis #MMPMID26618986 Araújo CV; Campbell C; Gonçalves-de-Albuquerque CF; Molinaro R; Cody MJ; Yost CC; Bozza PT; Zimmerman GA; Weyrich AS; Castro-Faria-Neto HC; Silva AR Shock 2016[Apr]; 45 (4): 393-403 PMID26618986show ga Dysregulation of the inflammatory response against infection contributes to mortality in sepsis. Inflammation provides critical host defense, but it can cause tissue damage, multiple organ failure and death. Because the nuclear transcription factor peroxisome proliferator-activated receptor ? (PPAR?) exhibits therapeutic potential, we characterized the role of PPAR? in sepsis. We analyzed severity of clinical signs, survival rates, cytokine production, leukocyte influx, and bacterial clearance in a cecal ligation and puncture (CLP) model of sepsis in Swiss mice. The PPAR? agonist rosiglitazone treatment improved clinical status and mortality, while increasing IL-10 production and decreasing TNF-? and IL-6 levels, and peritoneal neutrophil accumulation 24 h after CLP. We noted increased bacterial killing in rosiglitazone treated mice, correlated with increased generation of reactive oxygen species. Polymorphonuclear leukocytes (PMN) incubated with LPS or E. coli and rosiglitazone increased peritoneal neutrophil extracellular trap (NET)-mediated bacterial killing, an effect reversed by the PPAR? antagonist (GW 9662) treatment. Rosiglitazone also enhanced the release of histones by PMN, a surrogate marker of NET formation, effect abolished by GW 9662. Rosiglitazone modulated the inflammatory response and increased bacterial clearance through PPAR? activation and NET formation, combining immunomodulatory and host-dependent anti-bacterial effects and, therefore, warrants further study as a potential therapeutic agent in sepsis. äA PPAR? agonist enhances bacterial clearance through neutrophil extrac(epmc).pdf DeepDyve Pubget Overpricing