The NLRP12 Inflammasome Recognizes Yersinia pestis
dc.contributor.author | Vladimer, Gregory I. | |
dc.contributor.author | Weng, Dan | |
dc.contributor.author | Paquette, Sara W. Montminy | |
dc.contributor.author | Vanaja, Sivapriya Kailasan | |
dc.contributor.author | Rathinam, Vijay A.K. | |
dc.contributor.author | Aune, Marie Hjelmseth | |
dc.contributor.author | Conlon, Joseph E. | |
dc.contributor.author | Burbage, Joseph J. | |
dc.contributor.author | Proulx, Megan K. | |
dc.contributor.author | Liu, Qin | |
dc.contributor.author | Reed, George W. | |
dc.contributor.author | Mecsas, Joan C. | |
dc.contributor.author | Iwakura, Yoichiro | |
dc.contributor.author | Bertin, John | |
dc.contributor.author | Goguen, Jon D. | |
dc.contributor.author | Fitzgerald, Katherine A | |
dc.contributor.author | Lien, Egil | |
dc.date | 2022-08-11T08:08:54.000 | |
dc.date.accessioned | 2022-08-23T16:11:46Z | |
dc.date.available | 2022-08-23T16:11:46Z | |
dc.date.issued | 2012-07-27 | |
dc.date.submitted | 2012-07-31 | |
dc.identifier.citation | <p>Immunity. 2012 Jul 27;37(1):96-107. DOI 10.1016/j.immuni.2012.07.006</p> | |
dc.identifier.issn | 1097-4180 | |
dc.identifier.doi | 10.1016/j.immuni.2012.07.006 | |
dc.identifier.pmid | 22840842 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/33248 | |
dc.description.abstract | Yersinia pestis, the causative agent of plague, is able to suppress production of inflammatory cytokines IL-18 and IL-1β, 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-1β production after Y. pestis infection, and NLRP12-deficient mice were more susceptible to bacterial challenge. NLRP12 also directed interferon-γ production via induction of IL-18, but had minimal effect on signaling to the transcription factor NF-κB. 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. | |
dc.language.iso | en_US | |
dc.publisher | Cell Press | |
dc.relation | <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=22840842&dopt=Abstract">Link to article in PubMed</a> | |
dc.relation.url | http://dx.doi.org/10.1016/j.immuni.2012.07.006 | |
dc.title | The NLRP12 Inflammasome Recognizes Yersinia pestis | |
dc.type | Journal Article | |
dc.source.journaltitle | Immunity | |
dc.source.volume | 37 | |
dc.source.issue | 1 | |
dc.identifier.legacyfulltext | https://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2792&context=gsbs_sp&unstamped=1 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/gsbs_sp/1782 | |
dc.identifier.contextkey | 3161834 | |
refterms.dateFOA | 2022-08-23T16:11:46Z | |
html.description.abstract | <p><em>Yersinia pestis</em>, the causative agent of plague, is able to suppress production of inflammatory cytokines IL-18 and IL-1β, 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 <em>Y. pestis</em>, 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-1β production after<em> Y. pestis</em> infection, and NLRP12-deficient mice were more susceptible to bacterial challenge. NLRP12 also directed interferon-γ production via induction of IL-18, but had minimal effect on signaling to the transcription factor NF-κB. 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 <em>Y. pestis</em>.</p> | |
dc.identifier.submissionpath | gsbs_sp/1782 | |
dc.contributor.department | Department of Medicine, Division of Preventive and Behavioral Medicine | |
dc.contributor.department | Department of Molecular Genetics and Microbiology | |
dc.contributor.department | Department of Medicine, Division of Infectious Disease and Immunology | |
dc.source.pages | 96-107 | |
dc.contributor.student | Gregory I. Vladimer; Dan Weng |