Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1371/journal.ppat.1004820 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1004820 C4399879!4399879!25880560     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       PLoS+Pathog 2015 ; 11 (4): ä Nephropedia Template TP {{tp|p=25880560|t=2015. Toxin-Induced Necroptosis Is a Major Mechanism of Staphylococcus aureus Lung Damage |pdf=|usr=}}{{25880560}} gab.com Text Toxin-Induced Necroptosis Is a Major Mechanism of Staphylococcus aureus Lung Damage JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=25880560 #FOAvip Staphylococcus aureus USA300 strains cause a highly inflammatory necrotizing pneumonia. The virulence of this strain has been attributed to its expression of multiple toxins that have diverse targets including ADAM10, NLRP3 and CD11b. We demonstrate that induction of necroptosis through RIP1/RIP3/MLKL signaling is a major consequence of S. aureus toxin production. Cytotoxicity could be prevented by inhibiting either RIP1 or MLKL signaling and S. aureus mutants lacking agr, hla or Hla pore formation, lukAB or psms were deficient in inducing cell death in human and murine immune cells. Toxin-associated pore formation was essential, as cell death was blocked by exogenous K+ or dextran. MLKL inhibition also blocked caspase-1 and IL-1? production, suggesting a link to the inflammasome. Rip3-/- mice exhibited significantly improved staphylococcal clearance and retained an alveolar macrophage population with CD200R and CD206 markers in the setting of acute infection, suggesting increased susceptibility of these leukocytes to necroptosis. The importance of this anti-inflammatory signaling was indicated by the correlation between improved outcome and significantly decreased expression of KC, IL-6, TNF, IL-1? and IL-1? in infected mice. These findings indicate that toxin-induced necroptosis is a major cause of lung pathology in S. aureus pneumonia and suggest the possibility of targeting components of this signaling pathway as a therapeutic strategy. Twit Text FOAVip Toxin-Induced Necroptosis Is a Major Mechanism of Staphylococcus aureus Lung Damage ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=25880560 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25880560 #FOAvip English Wikipedia <ref>{{Cite pmid|25880560}}</ref> Toxin-Induced Necroptosis Is a Major Mechanism of Staphylococcus aureus Lung Damage #MMPMID25880560 Kitur K; Parker D; Nieto P; Ahn DS; Cohen TS; Chung S; Wachtel S; Bueno S; Prince A PLoS Pathog 2015[Apr]; 11 (4): ä PMID25880560show ga Staphylococcus aureus USA300 strains cause a highly inflammatory necrotizing pneumonia. The virulence of this strain has been attributed to its expression of multiple toxins that have diverse targets including ADAM10, NLRP3 and CD11b. We demonstrate that induction of necroptosis through RIP1/RIP3/MLKL signaling is a major consequence of S. aureus toxin production. Cytotoxicity could be prevented by inhibiting either RIP1 or MLKL signaling and S. aureus mutants lacking agr, hla or Hla pore formation, lukAB or psms were deficient in inducing cell death in human and murine immune cells. Toxin-associated pore formation was essential, as cell death was blocked by exogenous K+ or dextran. MLKL inhibition also blocked caspase-1 and IL-1? production, suggesting a link to the inflammasome. Rip3-/- mice exhibited significantly improved staphylococcal clearance and retained an alveolar macrophage population with CD200R and CD206 markers in the setting of acute infection, suggesting increased susceptibility of these leukocytes to necroptosis. The importance of this anti-inflammatory signaling was indicated by the correlation between improved outcome and significantly decreased expression of KC, IL-6, TNF, IL-1? and IL-1? in infected mice. These findings indicate that toxin-induced necroptosis is a major cause of lung pathology in S. aureus pneumonia and suggest the possibility of targeting components of this signaling pathway as a therapeutic strategy. äToxin-Induced Necroptosis Is a Major Mechanism of Staphylococcus aureu(epmc).pdf DeepDyve Pubget Overpricing