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dc.contributor.authorCoutermarsh-Ott, Sheryl L.en_US
dc.contributor.authorDoran, John T.en_US
dc.contributor.authorCampbell, Carolineen_US
dc.contributor.authorWilliams, Tere M.en_US
dc.contributor.authorLindsay, David S.en_US
dc.contributor.authorAllen, Irving C.en_US
dc.date.accessioned2017-03-26T19:19:56Z
dc.date.available2017-03-26T19:19:56Z
dc.date.issued2016-06-09en_US
dc.identifier.citationSheryl L. Coutermarsh-Ott, John T. Doran, Caroline Campbell, Tere M. Williams, David S. Lindsay, and Irving C. Allen, “Caspase-11 Modulates Inflammation and Attenuates Toxoplasma gondii Pathogenesis,” Mediators of Inflammation, vol. 2016, Article ID 9848263, 14 pages, 2016. doi:10.1155/2016/9848263
dc.identifier.issn0962-9351en_US
dc.identifier.urihttp://hdl.handle.net/10919/76684
dc.description.abstractToxoplasma gondii is an obligate intracellular parasite that is the etiologic agent responsible for toxoplasmosis. Infection with T. gondii results in activation of nucleotide binding domain and leucine rich repeat containing receptors (NLRs). NLR activation leads to inflammasome formation, the activation of caspase-1, and the subsequent cleavage of IL-1β and IL-18. Recently, a noncanonical inflammasome has been characterized which functions through caspase-11 and appears to augment many biological functions previously considered to be dependent upon the canonical inflammasome. To better elucidate the function of this noncanonical inflammasome in toxoplasmosis, we utilized Asc−/− and Casp11−/− mice and infected these animals with T. gondii. Our data indicates that caspase-11 modulates the innate immune response to T. gondii through a mechanism which is distinct from that currently described for the canonical inflammasome. Asc−/− mice demonstrated increased disease pathogenesis during the acute phase of T. gondii infection, whereas Casp11−/− mice demonstrated significantly attenuated disease pathogenesis and reduced inflammation. This attenuated host response was associated with reduced local and systemic cytokine production, including diminished IL-1β. During the chronic phase of infection, caspase-11 deficiency resulted in increased neuroinflammation and tissue cyst burden in the brain. Together, our data suggest that caspase-11 functions to protect the host by enhancing inflammation during the early phase of infection in an effort to minimize disease pathogenesis during later stages of toxoplasmosis.en_US
dc.format.extent? - ? (14) page(s)en_US
dc.format.mimetypeapplication/pdf
dc.languageEnglishen_US
dc.publisherHindawi Publishing Corpen_US
dc.relation.urihttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000378570900001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=930d57c9ac61a043676db62af60056c1en_US
dc.rightsCreative Commons Attribution 4.0 International (CC BY 4.0)*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCell Biologyen_US
dc.subjectImmunologyen_US
dc.subjectDENDRITIC CELLSen_US
dc.subjectNLRP3 INFLAMMASOMEen_US
dc.subjectGAMMA-INTERFERONen_US
dc.subjectIMMUNE-RESPONSEen_US
dc.subjectINFECTIONen_US
dc.subjectACTIVATIONen_US
dc.subjectRECEPTORen_US
dc.subjectINNATEen_US
dc.subjectRESISTANCEen_US
dc.subjectMYD88en_US
dc.titleCaspase-11 Modulates Inflammation and Attenuates Toxoplasma gondii Pathogenesisen_US
dc.typeArticle - Refereed
dc.description.versionPublished (Publication status)en_US
dc.rights.holderCopyright © 2016 Sheryl L. Coutermarsh-Ott et al.en_US
dc.title.serialMEDIATORS OF INFLAMMATIONen_US
dc.identifier.doihttps://doi.org/10.1155/2016/9848263
dc.identifier.orcidAllen, IC [0000-0001-9573-5250]en_US
dc.rights.licenseThis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
pubs.organisational-group/Virginia Tech
pubs.organisational-group/Virginia Tech/All T&R Faculty
pubs.organisational-group/Virginia Tech/Faculty of Health Sciences
pubs.organisational-group/Virginia Tech/Veterinary Medicine
pubs.organisational-group/Virginia Tech/Veterinary Medicine/Biomedical Sciences and Pathobiology
pubs.organisational-group/Virginia Tech/Veterinary Medicine/CVM T&R Faculty


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Creative Commons Attribution 4.0 International (CC BY 4.0)
License: Creative Commons Attribution 4.0 International (CC BY 4.0)