| First Author | Muñoz-Planillo R | Year | 2013 |
| Journal | Immunity | Volume | 38 |
| Issue | 6 | Pages | 1142-53 |
| PubMed ID | 23809161 | Mgi Jnum | J:207576 |
| Mgi Id | MGI:5559133 | Doi | 10.1016/j.immuni.2013.05.016 |
| Citation | Munoz-Planillo R, et al. (2013) K(+) efflux is the common trigger of NLRP3 inflammasome activation by bacterial toxins and particulate matter. Immunity 38(6):1142-53 |
| abstractText | The NLRP3 inflammasome is an important component of the innate immune system. However, its mechanism of activation remains largely unknown. We show that NLRP3 activators including bacterial pore-forming toxins, nigericin, ATP, and particulate matter caused mitochondrial perturbation or the opening of a large membrane pore, but this was not required for NLRP3 activation. Furthermore, reactive oxygen species generation or a change in cell volume was not necessary for NLRP3 activation. Instead, the only common activity induced by all NLRP3 agonists was the permeation of the cell membrane to K(+) and Na(+). Notably, reduction of the intracellular K(+) concentration was sufficient to activate NLRP3, whereas an increase in intracellular Na(+) modulated but was not strictly required for inflammasome activation. These results provide a unifying model for the activation of the NLRP3 inflammasome in which a drop in cytosolic K(+) is the common step that is necessary and sufficient for caspase-1 activation. |
