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dc.contributor.authorAutorHernández-Cabanyero, Carla
dc.contributor.authorAutorSanjuan, Eva
dc.contributor.authorAutorReyes-López, Felipe E.
dc.contributor.authorAutorVallejos-Vidal, Eva
dc.contributor.authorAutorLluis, Tort
dc.contributor.authorAutorAmaro, Carmen
dc.contributor.otherCarreraFacultad de medicina veterinaria y agronomíaes
dc.date.accessionedFecha ingreso2022-05-02T16:31:20Z
dc.date.availableFecha disponible2022-05-02T16:31:20Z
dc.date.issuedFecha publicación2022-04-01
dc.identifier.citationReferencia BibliográficaFrontiers in Microbiology 13,17 p.
dc.identifier.issnISSN1664-302X
dc.identifier.uriURLhttp://repositorio.udla.cl/xmlui/handle/udla/987
dc.identifier.uriURLhttps://www.frontiersin.org/journals/microbiology
dc.description.abstractResumenVibrio vulnificus is a marine zoonotic pathogen associated with fish farms that is considered a biomarker of climate change. Zoonotic strains trigger a rapid death of their susceptible hosts (fish or humans) by septicemia that has been linked to a cytokine storm in mice. Therefore, we hypothesize that V. vulnificus also causes fish death by triggering a cytokine storm in which red blood cells (RBCs), as nucleated cells in fish, could play an active role. To do it, we used the eel immersion infection model and then analyzed the transcriptome in RBCs, white BCs, and whole blood using an eel-specific microarray platform. Our results demonstrate that V. vulnificus triggers an acute but atypical inflammatory response that occurs in two main phases. The early phase (3 h post-infection [hpi]) is characterized by the upregulation of several genes for proinflammatory cytokines related to the mucosal immune response (il17a/f1 and il20) along with genes for antiviral cytokines (il12β) and antiviral factors (ifna and ifnc). In contrast, the late phase (12 hpi) is based on the upregulation of genes for typical inflammatory cytokines (il1β), endothelial destruction (mmp9 and hyal2), and, interestingly, genes related to an RNA-based immune response (sidt1). Functional assays revealed significant proteolytic and hemolytic activity in serum at 12 hpi that would explain the hemorrhages characteristic of this septicemia in fish. As expected, we found evidence that RBCs are transcriptionally active and contribute to this atypical immune response, especially in the short term. Based on a selected set of marker genes, we propose here an in vivo RT-qPCR assay that allows detection of early sepsis caused by V. vulnificus. Finally, we develop a model of sepsis that could serve as a basis for understanding sepsis caused by V. vulnificus not only in fish but also in humans.es
dc.format.extentdc.format.extent17 páginas
dc.format.extentdc.format.extent2.488Mb
dc.format.mimetypedc.format.mimetypePDF
dc.language.isoLenguaje ISOen
dc.publisherEditorFrontiers Media S.A.
dc.sourceFuentesFrontiers in Microbiology
dc.subjectPalabras ClavesVirbio vulnificuses
dc.subjectPalabras ClavesZoonotic pathogenes
dc.subjectPalabras ClavesEuropean eeles
dc.subjectPalabras ClavesHost-pathogen relationshipes
dc.subjectPalabras ClavesInmune responsees
dc.subject.lcshdc.subject.lcshBlood
dc.subject.lcshdc.subject.lcshErythrocytes
dc.titleTítuloA Transcriptomic Study Reveals That Fish Vibriosis Due to the Zoonotic Pathogen Vibrio vulnificus Is an Acute Inflammatory Disease in Which Erythrocytes May Play an Important Rolees
dc.typeTipo de DocumentoArtículoes
dc.udla.catalogadordc.udla.catalogadorCBM
dc.udla.indexdc.udla.indexSCOPUS
dc.identifier.doidc.identifier.doihttps://doi.org/10.3389/fmicb.2022.852677
dc.udla.privacidaddc.udla.privacidadDocumento públicoes


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