Characterization of NLRP12 during the Development of Allergic Airway Disease in Mice

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dc.contributor.authorAllen, Irving C.en
dc.contributor.authorLich, John D.en
dc.contributor.authorArthur, Janelle C.en
dc.contributor.authorJania, Corey M.en
dc.contributor.authorRoberts, Reid A.en
dc.contributor.authorCallaway, Justin B.en
dc.contributor.authorTilley, Stephen L.en
dc.contributor.authorTing, Jenny P.-Y.en
dc.date.accessioned2017-01-10T00:49:19Zen
dc.date.available2017-01-10T00:49:19Zen
dc.date.issued2012-01-23en
dc.description.abstractAmong the 22 members of the nucleotide binding-domain, leucine rich repeat-containing (NLR) family, less than half have been functionally characterized. Of those that have been well studied, most form caspase-1 activating inflammasomes. NLRP12 is a unique NLR that has been shown to attenuate inflammatory pathways in biochemical assays and mediate the lymph node homing of activated skin dendritic cells in contact hypersensitivity responses. Since the mechanism between these two important observations remains elusive, we further evaluated the contribution of NLRP12 to organ specific adaptive immune responses by focusing on the lung, which, like skin, is exposed to both exogenous and endogenous inflammatory agents. In models of allergic airway inflammation induced by either acute ovalbumin (OVA) exposure or chronic house dust mite (HDM) antigen exposure, Nlrp122/2 mice displayed subtle differences in eosinophil and monocyte infiltration into the airways. However, the overall development of allergic airway disease and airway function was not significantly altered by NLRP12 deficiency. Together, the combined data suggest that NLRP12 does not play a vital role in regulating Th2 driven airway inflammation using common model systems that are physiologically relevant to human disease. Thus, the allergic airway inflammation models described here should be appropriate for subsequent studies that seek to decipher the contribution of NLRP12 in mediating the host response to agents associated with asthma exacerbation.en
dc.description.versionPublished versionen
dc.format.extent? - ? (9) page(s)en
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0030612en
dc.identifier.issn1932-6203en
dc.identifier.issue1en
dc.identifier.urihttp://hdl.handle.net/10919/74044en
dc.identifier.volume7en
dc.language.isoenen
dc.publisherPLOSen
dc.relation.urihttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000301570600063&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.subjectnf-kappa-ben
dc.subjectcutting edgeen
dc.subjectin-vivoen
dc.subjectsignaling pathwaysen
dc.subjectproteinen
dc.subjectactivationen
dc.subjectmonarch-1en
dc.subjectgenesen
dc.subjectcellsen
dc.subjectcaterpilleren
dc.titleCharacterization of NLRP12 during the Development of Allergic Airway Disease in Miceen
dc.title.serialPLOS ONEen
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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