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A mouse model reproducing the pathophysiology of neonatal group B streptococcal infection

dc.contributor.authorBonifácio Andrade, Elva
dc.contributor.authorMagalhães, Ana
dc.contributor.authorPuga, Ana
dc.contributor.authorCosta, Madalena
dc.contributor.authorBravo, Joana
dc.contributor.authorPortugal, Camila Cabral
dc.contributor.authorRibeiro, Adília
dc.contributor.authorCorreia-Neves, Margarida
dc.contributor.authorFaustino, Augusto
dc.contributor.authorFiron, Arnaud
dc.contributor.authorTrieu-Cuot, Patrick
dc.contributor.authorSummavielle, Teresa
dc.contributor.authorFerreira, Paula
dc.date.accessioned2019-05-17T16:52:06Z
dc.date.available2019-05-17T16:52:06Z
dc.date.issued2018
dc.description.abstractGroup B streptococcal (GBS) meningitis remains a devastating disease. The absence of an animal model reproducing the natural infectious process has limited our understanding of the disease and, consequently, delayed the development of effective treatments. We describe here a mouse model in which bacteria are transmitted to the offspring from vaginally colonised pregnant females, the natural route of infection. We show that GBS strain BM110, belonging to the CC17 clonal complex, is more virulent in this vertical transmission model than the isogenic mutant BM110∆cylE, which is deprived of hemolysin/cytolysin. Pups exposed to the more virulent strain exhibit higher mortality rates and lung inflammation than those exposed to the attenuated strain. Moreover, pups that survive to BM110 infection present neurological developmental disability, revealed by impaired learning performance and memory in adulthood. The use of this new mouse model, that reproduces key steps of GBS infection in newborns, will promote a better understanding of the physiopathology of GBS-induced meningitis.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationAndrade, E.B., Magalhães, A., Puga, A. et al. A mouse model reproducing the pathophysiology of neonatal group B streptococcal infection (2018). Nat Commun 9, 3138. https://doi.org/10.1038/s41467-018-05492-y
dc.identifier.doi10.1038/s41467-018-05492-ypt_PT
dc.identifier.urihttp://hdl.handle.net/10400.22/13734
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationPOCI-01-0145-FEDER-016607pt_PT
dc.relation.publisherversionhttps://www.nature.com/articles/s41467-018-05492-ypt_PT
dc.subjectAnimalspt_PT
dc.subjectBehavior, Animalpt_PT
dc.subjectBody Weightpt_PT
dc.subjectHemolysin Proteinspt_PT
dc.subjectInflammationpt_PT
dc.subjectMaze Learningpt_PT
dc.subjectMeningitispt_PT
dc.subjectMeningitis, Bacterialpt_PT
dc.subjectMicept_PT
dc.subjectMice, Inbred BALB Cpt_PT
dc.subjectPerforinpt_PT
dc.subjectPregnancypt_PT
dc.subjectPregnancy, Animalpt_PT
dc.subjectStreptococcal Infectionspt_PT
dc.subjectStreptococcus agalactiaept_PT
dc.subjectDisease Models, Animalpt_PT
dc.subjectInfectious Disease Transmission, Verticalpt_PT
dc.titleA mouse model reproducing the pathophysiology of neonatal group B streptococcal infectionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue1pt_PT
oaire.citation.startPage3138pt_PT
oaire.citation.titleNature Communicationspt_PT
oaire.citation.volume9pt_PT
person.familyNameBonifácio Andrade
person.familyNameBravo
person.familyNameSummavielle
person.givenNameElva
person.givenNameJoana
person.givenNameTeresa
person.identifier677706
person.identifier.ciencia-id511C-11AA-7980
person.identifier.ciencia-idAA15-F362-062E
person.identifier.ciencia-idC41E-0816-5C85
person.identifier.orcid0000-0002-1941-580X
person.identifier.orcid0000-0002-8403-7235
person.identifier.orcid0000-0003-2548-6281
person.identifier.ridC-9776-2012
person.identifier.scopus-author-id6603092949
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicatione3b8883f-57b2-4b83-afa1-88e663ed8d1f
relation.isAuthorOfPublication617f0f54-58dd-45b8-a90f-177187cd197e
relation.isAuthorOfPublication207ee2de-85a0-4144-9e7e-b376c600e065
relation.isAuthorOfPublication.latestForDiscoverye3b8883f-57b2-4b83-afa1-88e663ed8d1f

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