| First Author | Aachoui Y | Year | 2015 |
| Journal | Cell Host Microbe | Volume | 18 |
| Issue | 3 | Pages | 320-32 |
| PubMed ID | 26320999 | Mgi Jnum | J:243015 |
| Mgi Id | MGI:5907423 | Doi | 10.1016/j.chom.2015.07.016 |
| Citation | Aachoui Y, et al. (2015) Canonical Inflammasomes Drive IFN-gamma to Prime Caspase-11 in Defense against a Cytosol-Invasive Bacterium. Cell Host Microbe 18(3):320-32 |
| abstractText | The inflammatory caspases 1 and 11 are activated in response to different agonists and act independently to induce pyroptosis. In the context of IL-1beta/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-gamma 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-gamma. Whereas IFN-gamma 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-gamma priming. Thus, caspase-1 provides priming signals upstream of caspase-11 but not caspase-4 during murine defense against a cytosol-invasive bacterium. |
