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10.1016/j.chom.2015.07.016 http://scihub22266oqcxt.onion/10.1016/j.chom.2015.07.016 C4567510!4567510 !26320999     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 261.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26320999 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cell+Host+Microbe 2015 ; 18 (3 ): 320-32 Nephropedia Template TP {{tp|p=26320999 |t=2015. Canonical Inflammasomes Drive IFN-? to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium |pdf=|usr=}}{{26320999 }} gab.com Text Canonical Inflammasomes Drive IFN- to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium JO: Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=26320999 #FOAvip The inflammatory caspases 1 and 11 are activated in response to different agonists and act independently to induce pyroptosis. In the context of IL-1?/IL-18 secretion, however, in vitro studies indicate that caspase-11 acts upstream of NLRP3 and caspase-1. By contrast, studying infection in vivo by the cytosol-invasive bacterium Burkholderia thailandensis, we find that caspase-1 activity is required upstream of caspase-11 to control infection. Caspase-1-activated IL-18 induces IFN-? to prime caspase-11 and rapidly clear B. thailandensis infection. In the absence of IL-18, bacterial burdens persist, eventually triggering other signals that induce IFN-?. Whereas IFN-? was essential, endogenous type I interferons were insufficient to prime caspase-11. Although mice transgenic for caspase-4, the human ortholog of caspase-11, cleared B. thailandensis in vivo, they did not strictly require IFN-? priming. Thus, caspase-1 provides priming signals upstream of caspase-11 but not caspase-4 during murine defense against a cytosol-invasive bacterium. Twit Text FOAVip Canonical Inflammasomes Drive IFN- to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium ????Cell Host Microbe http://www.kidney.de/pget.php?&tw=1&pmid=26320999 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26320999 #FOAvip English Wikipedia <ref>{{Cite pmid|26320999 }}</ref> Canonical Inflammasomes Drive IFN-? to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium #MMPMID26320999 Aachoui Y ; Kajiwara Y ; Leaf IA ; Mao D ; Ting JP ; Coers J ; Aderem A ; Buxbaum JD ; Miao EA Cell Host Microbe 2015[Sep]; 18 (3 ): 320-32 PMID26320999 show ga The inflammatory caspases 1 and 11 are activated in response to different agonists and act independently to induce pyroptosis. In the context of IL-1?/IL-18 secretion, however, in vitro studies indicate that caspase-11 acts upstream of NLRP3 and caspase-1. By contrast, studying infection in vivo by the cytosol-invasive bacterium Burkholderia thailandensis, we find that caspase-1 activity is required upstream of caspase-11 to control infection. Caspase-1-activated IL-18 induces IFN-? to prime caspase-11 and rapidly clear B. thailandensis infection. In the absence of IL-18, bacterial burdens persist, eventually triggering other signals that induce IFN-?. Whereas IFN-? was essential, endogenous type I interferons were insufficient to prime caspase-11. Although mice transgenic for caspase-4, the human ortholog of caspase-11, cleared B. thailandensis in vivo, they did not strictly require IFN-? priming. Thus, caspase-1 provides priming signals upstream of caspase-11 but not caspase-4 during murine defense against a cytosol-invasive bacterium. |Animals [MESH] |Burkholderia/*immunology [MESH] |Caspase 1/*metabolism [MESH] |Caspases, Initiator/metabolism [MESH] |Caspases/*metabolism [MESH] |Cytosol/*microbiology [MESH] |Humans [MESH] |Inflammasomes/*metabolism [MESH] |Interferon-gamma/*metabolism [MESH] |Interleukin-18/*metabolism [MESH] |Mice [MESH] |Mice, Transgenic [MESH]Canonical Inflammasomes Drive IFN-? to Prime Caspase-11 in Defense aga(epmc).pdf DeepDyve Pubget Overpricing