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dc.contributor.authorChristaki, Eirinien
dc.contributor.authorOpal, Steven M.en
dc.contributor.authorJr, James C. Keithen
dc.contributor.authorKessimian, Nubaren
dc.contributor.authorPalardy, J. E.en
dc.contributor.authorParejo, N. A.en
dc.contributor.authorLaVallie, Edward R.en
dc.contributor.authorRacie, L.en
dc.contributor.authorMounts, W.en
dc.contributor.authorMalamas, Michael S.en
dc.contributor.authorMewshaw, Richard E.en
dc.contributor.authorHarris, Heather A.en
dc.contributor.authorVlasuk, G. P.en
dc.creatorChristaki, Eirinien
dc.creatorOpal, Steven M.en
dc.creatorJr, James C. Keithen
dc.creatorKessimian, Nubaren
dc.creatorPalardy, J. E.en
dc.creatorParejo, N. A.en
dc.creatorLaVallie, Edward R.en
dc.creatorRacie, L.en
dc.creatorMounts, W.en
dc.creatorMalamas, Michael S.en
dc.creatorMewshaw, Richard E.en
dc.creatorHarris, Heather A.en
dc.creatorVlasuk, G. P.en
dc.date.accessioned2018-06-22T09:52:49Z
dc.date.available2018-06-22T09:52:49Z
dc.date.issued2010
dc.identifier.urihttps://gnosis.library.ucy.ac.cy/handle/7/41524
dc.description.abstractBackground. Nonsteroidal agonists have been developed that selectively bind to and activate estrogen receptor β (ERβ) rather than estrogen receptor α (ERα). ERβ is expressed equally in both male and female mammals in multiple extragonadal tissues. Work reported elsewhere has demonstrated that ERβ agonists have beneficial effects in multiple (but not all) models of inflammatory diseases and also increase survival in experimentally induced sepsis. Methods. In these experiments, ERβ agonists (ERB-041 or WAY-202196) were compared with vehicle control in the murine cecal ligation and puncture (CLP) model and in the pneumococcal pneumonia model of sepsis. The effect of WAY-202196 on the gene expression profile in the CLP model was further studied by transcriptome analysis of lung and small intestine tissue samples. Results. ERβ agonists provided a significant survival benefit in both experimental models of bacterial sepsis. This survival advantage was accompanied by reduced histologic evidence of tissue damage, reduced transcription of multiple proinflammatory proteins by transcriptome analysis and was not associated with increased bacterial outgrowth. Conclusions. ERβ agonist administration provided a survival advantage in septic animals and appears to be a promising therapeutic modality in sepsis. © 2010 by the Infectious Diseases Society of America. All rights reserved.en
dc.language.isoengen
dc.sourceJournal of Infectious Diseasesen
dc.subjectArticleen
dc.subjectControlled studyen
dc.subjectFemaleen
dc.subjectPriority journalen
dc.subjectSurvivalen
dc.subjectMaleen
dc.subjectSepsisen
dc.subjectGeneticen
dc.subjectUnclassified drugen
dc.subjectNonhumanen
dc.subjectPneumoniaen
dc.subjectAnimalsen
dc.subjectMiceen
dc.subjectAnimalen
dc.subjectAnimal experimenten
dc.subjectAnimal modelen
dc.subjectAnimal tissueen
dc.subjectDisease modelsen
dc.subjectMouseen
dc.subjectPneumococcalen
dc.subjectStreptococcus pneumoniaen
dc.subjectGene expression profilingen
dc.subjectBacterial overgrowthen
dc.subjectCell protectionen
dc.subjectEstrogen receptor betaen
dc.subjectExperimental modelen
dc.subjectGenetic transcriptionen
dc.subjectHormone receptor stimulating agenten
dc.subjectInbred balb cen
dc.subjectLung parenchymaen
dc.subjectNaphtholsen
dc.subjectOxazolesen
dc.subjectPharmacogenomicsen
dc.subjectPrinaberelen
dc.subjectSmall intestineen
dc.subjectTissue injuryen
dc.subjectTranscriptionen
dc.subjectTranscription regulationen
dc.subjectTranscriptomeen
dc.subjectWay 202196en
dc.titleEstrogen receptor β agonism increases survival in experimentally induced sepsis and ameliorates the genomic sepsis signature: A pharmacogenomic studyen
dc.typeinfo:eu-repo/semantics/article
dc.identifier.doi10.1086/651276
dc.description.volume201
dc.description.issue8
dc.description.startingpage1250
dc.description.endingpage1257
dc.author.facultyΙατρική Σχολή / Medical School
dc.author.departmentΙατρική Σχολή / Medical School
dc.type.uhtypeArticleen
dc.contributor.orcidChristaki, Eirini [0000-0002-8152-6367]
dc.gnosis.orcid0000-0002-8152-6367


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