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dc.contributor.authorGupta, Rahul
dc.contributor.authorGhosh, Shubhendu
dc.contributor.authorMonks, Brian G.
dc.contributor.authorDeOliveira, Rosane B.
dc.contributor.authorTzeng, TeChen
dc.contributor.authorKalantari, Parisa
dc.contributor.authorNandy, Anubhab
dc.contributor.authorBhattacharjee, Bornali
dc.contributor.authorChan, Jennie
dc.contributor.authorFerreira, Fabianno
dc.contributor.authorRathinam, Vijay A.K.
dc.contributor.authorSharma, Shrutie
dc.contributor.authorLien, Egil
dc.contributor.authorSilverman, Neal S.
dc.contributor.authorFitzgerald, Katherine A.
dc.contributor.authorFiron, Arnaud
dc.contributor.authorTrieu-Cuot, Patrick
dc.contributor.authorHenneke, Philipp
dc.contributor.authorGolenbock, Douglas T.
dc.date2022-08-11T08:09:08.000
dc.date.accessioned2022-08-23T16:18:57Z
dc.date.available2022-08-23T16:18:57Z
dc.date.issued2014-04-01
dc.date.submitted2014-04-15
dc.identifier.citationGupta R, Ghosh S, Monks B, Deoliveira R, Tzeng T, Kalantari P, Nandy A, Bhattacharjee B, Chan J, Ferreira F, Rathinam V, Sharma S, Lien E, Silverman N, Fitzgerald K, Firon A, Trieu-Cuot P, Henneke P, Golenbock D. RNA and β-hemolysin of Group B streptococcus induce IL-1β by activating NLRP3 inflammasomes in mouse macrophages. J Biol Chem. 2014 Apr 1. doi:10.1074/jbc.C114.548982. <a href="http://dx.doi.org/10.1074/jbc.C114.548982" target="_blank"> Link to article on publisher's site</a>
dc.identifier.issn0021-9258 (Linking)
dc.identifier.doi10.1074/jbc.C114.548982
dc.identifier.pmid24692555
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34934
dc.descriptionCo-authors Anubhab Nandy and Jennie Chan are doctoral students in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.
dc.description.abstractThe inflammatory cytokine IL-1beta is critical for host responses against many human pathogens. Here, we define Group B streptococcus (GBS)-mediated activation of the Nod-like Receptor-P3 (NLRP3) inflammasome in macrophages. NLRP3 activation requires GBS expression of the cytolytic toxin, beta-hemolysin, lysosomal acidification, and leakage. These processes allow the interaction of GBS RNA with cytosolic NLRP3. The present study supports a model in which GBS RNA, along with lysosomal components including cathepsins, leaks out of lysosomes and interacts with NLRP3 to induce IL-1beta production.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24692555&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1074/jbc.C114.548982
dc.subjectCell signaling
dc.subjectImmunology
dc.subjectInnate immunity
dc.subjectInterleukin
dc.subjectRNA
dc.subjectBacterial Infections and Mycoses
dc.subjectBiochemistry
dc.subjectImmunity
dc.subjectImmunology and Infectious Disease
dc.subjectImmunology of Infectious Disease
dc.titleRNA and beta-hemolysin of Group B streptococcus induce IL-1beta by activating NLRP3 inflammasomes in mouse macrophages
dc.typeJournal Article
dc.source.journaltitleThe Journal of biological chemistry
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/158
dc.identifier.contextkey5483052
html.description.abstract<p>The inflammatory cytokine IL-1beta is critical for host responses against many human pathogens. Here, we define Group B streptococcus (GBS)-mediated activation of the Nod-like Receptor-P3 (NLRP3) inflammasome in macrophages. NLRP3 activation requires GBS expression of the cytolytic toxin, beta-hemolysin, lysosomal acidification, and leakage. These processes allow the interaction of GBS RNA with cytosolic NLRP3. The present study supports a model in which GBS RNA, along with lysosomal components including cathepsins, leaks out of lysosomes and interacts with NLRP3 to induce IL-1beta production.</p>
dc.identifier.submissionpathinfdis_pp/158
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology


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