| First Author | Vladimer GI | Year | 2012 |
| Journal | Immunity | Volume | 37 |
| Issue | 1 | Pages | 96-107 |
| PubMed ID | 22840842 | Mgi Jnum | J:187388 |
| Mgi Id | MGI:5436347 | Doi | 10.1016/j.immuni.2012.07.006 |
| Citation | Vladimer GI, et al. (2012) The NLRP12 inflammasome recognizes Yersinia pestis. Immunity 37(1):96-107 |
| abstractText | Yersinia pestis, the causative agent of plague, is able to suppress production of inflammatory cytokines IL-18 and IL-1beta, which are generated through caspase-1-activating nucleotide-binding domain and leucine-rich repeat (NLR)-containing inflammasomes. Here, we sought to elucidate the role of NLRs and IL-18 during plague. Lack of IL-18 signaling led to increased susceptibility to Y. pestis, producing tetra-acylated lipid A, and an attenuated strain producing a Y. pseudotuberculosis-like hexa-acylated lipid A. We found that the NLRP12 inflammasome was an important regulator controlling IL-18 and IL-1beta production after Y. pestis infection, and NLRP12-deficient mice were more susceptible to bacterial challenge. NLRP12 also directed interferon-gamma production via induction of IL-18, but had minimal effect on signaling to the transcription factor NF-kappaB. These studies reveal a role for NLRP12 in host resistance against pathogens. Minimizing NLRP12 inflammasome activation may have been a central factor in evolution of the high virulence of Y. pestis. |
