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CXCL10-dependent epithelial-vascular cross-talk for endothelial activation following Sars-CoV-2 infection

dc.rights.licenseopenen_US
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorCHAILLOT, Laura
hal.structure.identifierMicrobiologie Fondamentale et Pathogénicité [MFP]
dc.contributor.authorBLONDOT, Marie-Lise
hal.structure.identifierMicrobiologie Fondamentale et Pathogénicité [MFP]
dc.contributor.authorRECORDON-PINSON, Patricia
hal.structure.identifierCentre Hospitalier Universitaire de Bordeaux [CHU Bordeaux]
dc.contributor.authorPELLEGRIN, Isabelle
hal.structure.identifierCentre Hospitalier Universitaire de Bordeaux [CHU Bordeaux]
dc.contributor.authorBOIZARD-MORACCHINI, Andrea
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorSLIUSAR, Myroslava
hal.structure.identifierUniversité de Bordeaux [UB]
dc.contributor.authorPUJOL, Nadège
hal.structure.identifierMicrobiologie Fondamentale et Pathogénicité [MFP]
dc.contributor.authorANDREOLA, Marie-Line
hal.structure.identifierBordeaux population health [BPH]
hal.structure.identifierGlobal Health in the Global South [GHiGS]
dc.contributor.authorBONNET, Fabrice
ORCID: 0000-0001-5927-4178
IDREF: 60714034
hal.structure.identifierLaboratoire Photonique, Numérique et Nanosciences [LP2N]
dc.contributor.authorRECHER, Gaelle
hal.structure.identifierTBM-Core [Bordeaux] [UMS3427 - INSERM US005]
dc.contributor.authorANDRIQUE, Leatitia
hal.structure.identifierLaboratoire Photonique, Numérique et Nanosciences [LP2N]
dc.contributor.authorNASSOY, Pierre
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorMATHIVET, Thomas
hal.structure.identifierBoRdeaux Institute in onCology [Inserm U1312 - BRIC]
dc.contributor.authorBIKFALVI, Andreas
dc.date.accessioned2024-10-24T12:18:17Z
dc.date.available2024-10-24T12:18:17Z
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/202709
dc.description.abstractEnAbstract The vasculature is heavily impacted by SARS-CoV-2 infection. Conflicting results exist concerningthe mechanisms by which the SARS-CoV-2 virus acts on the vasculature. The presence of the virus within endothelial cells has been reported in patient samples. However, the ACE2 receptor wasnot detected in endothelial cells when analyzed by RNAseq analysis. Thus, how SARS-CoV-2 contributes to vascular inflammation and whether cross-talk between epithelial cells and endothelial cells is involvedare unclear. Therefore, we investigated the interaction between SARS-CoV-2 and the vasculature using 2D and 3D in vitro models, as well asour previously developed 3D vesseloid model. We first determined the suitability of the 3D vesseloid model for our study and then assessed whether SARS-CoV-2 is able to directly infect endothelial cells. In the absence of ACE2 in endothelial cells, no infection was detected. When ACE2 was overexpressed in endothelial cells, low uptake of viral particles by endothelial cells was observed without efficient viral production. We then explored the possibility that an indirect effect of SARS-CoV-2 infection involvesepithelial-endothelial cellcross-talk. After infection of the epithelial cells, a significant inflammatory response was detected in the endothelial cells. Furthermore, we investigated the cytokines possibly implicated and identified CXCL10 as the most highly expressed proinflammatorycytokine and explored its function in this context. Finally, the clinical relevance of our findings was confirmed by evaluating CXCL10 and alternative cytokine dosages in blood samples fromSARS-CoV-2-infected patients, which were validated in silico in an independent patient cohort.
dc.description.sponsorshipLe Vesseloid enflammé sur puce - ANR-21-CE19-0029en_US
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enEndothelium
dc.subject.enSars-Cov-2
dc.subject.enChemokines
dc.subject.enCXCL10
dc.title.enCXCL10-dependent epithelial-vascular cross-talk for endothelial activation following Sars-CoV-2 infection
dc.typeDocument de travail - Pré-publicationen_US
dc.identifier.doi10.21203/rs.3.rs-3914352/v2en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - UMR 1219en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.institutionCNRS
bordeaux.teamGHIGS_BPHen_US
bordeaux.identifier.funderIDInstitut de Recherche pour le Développementen_US
bordeaux.identifier.funderIDFondation pour la Recherche Médicaleen_US
bordeaux.import.sourcehal
hal.identifierhal-04741709
hal.version1
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
workflow.import.sourcehal
dc.rights.ccPas de Licence CCen_US
bordeaux.subtypePrepublication/Preprinten_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.au=CHAILLOT,%20Laura&BLONDOT,%20Marie-Lise&RECORDON-PINSON,%20Patricia&PELLEGRIN,%20Isabelle&BOIZARD-MORACCHINI,%20Andrea&rft.genre=preprint


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