Nonessential Role for the NLRP1 Inflammasome Complex in a Murine Model of Traumatic Brain Injury

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dc.contributor.authorBrickler, Thomasen
dc.contributor.authorGresham, Kishaen
dc.contributor.authorMeza, Armanden
dc.contributor.authorCoutermarsh-Ott, Sherylen
dc.contributor.authorWilliams, Tere M.en
dc.contributor.authorRothschild, Daniel E.en
dc.contributor.authorAllen, Irving C.en
dc.contributor.authorTheus, Michelle H.en
dc.date.accessioned2017-01-24T13:51:29Zen
dc.date.available2017-01-24T13:51:29Zen
dc.date.issued2016-01-01en
dc.description.abstractTraumatic brain injury (TBI) elicits the immediate production of proinflammatory cytokines which participate in regulating the immune response. While the mechanisms of adaptive immunity in secondary injury are well characterized, the role of the innate response is unclear. Recently, the NLR inflammasome has been shown to become activated following TBI, causing processing and release of interleukin-1β (IL-1β). The inflammasome is a multiprotein complex consisting of nucleotide-binding domain and leucine-rich repeat containing proteins (NLR), caspase-1, and apoptosis-associated speck-like protein (ASC). ASC is upregulated after TBI and is critical in coupling the proteins during complex formation resulting in IL-1β cleavage. To directly test whether inflammasome activation contributes to acute TBI-induced damage, we assessed IL-1β, IL-18, and IL-6 expression, contusion volume, hippocampal cell death, and motor behavior recovery in Nlrp1−/−, Asc−/−, and wild type mice after moderate controlled cortical impact (CCI) injury. Although IL-1β expression is significantly attenuated in the cortex of Nlrp1−/− and Asc−/− mice following CCI injury, no difference in motor recovery, cell death, or contusion volume is observed compared to wild type. These findings indicate that inflammasome activation does not significantly contribute to acute neural injury in the murine model of moderate CCI injury.en
dc.description.versionPublished versionen
dc.format.extent? - ? (11) page(s)en
dc.format.mimetypeapplication/pdfen
dc.identifier.citationThomas Brickler, Kisha Gresham, Armand Meza, Sheryl Coutermarsh-Ott, Tere M. Williams, Daniel E. Rothschild, Irving C. Allen, Michelle H. Theus, "Nonessential Role for the NLRP1 Inflammasome Complex in a Murine Model of Traumatic Brain Injury", Mediators of Inflammation, vol. 2016, Article ID 6373506, 11 pages, 2016. https://doi.org/10.1155/2016/6373506en
dc.identifier.doihttps://doi.org/10.1155/2016/6373506en
dc.identifier.issn0962-9351en
dc.identifier.urihttp://hdl.handle.net/10919/74412en
dc.language.isoenen
dc.publisherHindawien
dc.relation.urihttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000375310700001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=930d57c9ac61a043676db62af60056c1en
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectCell Biologyen
dc.subjectImmunologyen
dc.subjectCONTROLLED CORTICAL IMPACTen
dc.subjectNECROSIS-FACTOR-ALPHAen
dc.subjectINTERLEUKIN-1 RECEPTOR ANTAGONISTen
dc.subjectEXCITOTOXIC NEURONAL DAMAGEen
dc.subjectNEURAL PROGENITOR CELLSen
dc.subjectNF-KAPPA-Ben
dc.subjectRAT-BRAINen
dc.subjectSUBVENTRICULAR ZONEen
dc.subjectNEGATIVE REGULATIONen
dc.subjectMESSENGER-RNAen
dc.titleNonessential Role for the NLRP1 Inflammasome Complex in a Murine Model of Traumatic Brain Injuryen
dc.title.serialMediators of Inflammationen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/Veterinary Medicineen
pubs.organisational-group/Virginia Tech/Veterinary Medicine/Biomedical Sciences and Pathobiologyen
pubs.organisational-group/Virginia Tech/Veterinary Medicine/CVM T&R Facultyen

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