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10.1016/j.chom.2015.07.016

http://scihub22266oqcxt.onion/10.1016/j.chom.2015.07.016
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suck abstract from ncbi


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pmid26320999      Cell+Host+Microbe 2015 ; 18 (3): 320-32
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  • 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 JPY; Coers J; Aderem A; Buxbaum JD; Miao EA
  • Cell Host Microbe 2015[Sep]; 18 (3): 320-32 PMID26320999show 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 orthologue 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.
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