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dc.rights.licenseopenen_US
dc.contributor.authorPREVEL, Renaud
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGARCIA, GEOFFREY
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCOLOMER, Sylvie
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorDUVIGNAUD, Alexandre
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
dc.contributor.authorCLEQUIN, Etienne
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDUSSIAU, Charles
hal.structure.identifierBordeaux population health [BPH]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorTREGOUET, David-Alexandre
hal.structure.identifierBordeaux population health [BPH]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
hal.structure.identifierGlobal Health in the Global South [GHiGS]
dc.contributor.authorMALVY, Denis
ORCID: 0000-0003-1948-9355
IDREF: 148480993
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGORET, Julien
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorMAMANI MATSUDA, Maria
IDREF: 060241373
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDEWITTE, Antoine
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorJAMES, Chloe
dc.date.accessioned2024-02-14T13:10:57Z
dc.date.available2024-02-14T13:10:57Z
dc.date.issued2023-09-09
dc.date.conference2023-09-09
dc.identifier.issn0903-1936en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/188129
dc.description.abstractEnBackground: Immunothrombosis is increased in severe COVID-19 and potentially involved in its pathogenesis but the mechanisms explaining its regulation are unknown. We hypothesized that decreased DNase activity could be associated with increased NETosis and clinical worsening in COVID-19 patients. Our objectives were to compare the balance between NETs biomarkers and DNase activity according to the severity of COVID-19 and to study the mechanisms responsible for the imbalance between NETosis and DNase activity. Methods: Biological samples were collected from the COLCOV19-BX study for inpatients and the COVERAGE trial (no treatment arm) for outpatients. We studied 93 non-severe, 15 severe and 37 critical COVID-19 patients. Results: Markers of NETs (MPO-DNA, H3Cit, H3cit-DNA) were higher in the most severe patients. DNase activity was lower and the balance between NET markers and DNase activity was impaired in the most severe patients. We observed a decrease in the amount of circulating DNase1 and DNase1L3 without mutations in the DNase1 and DNase1L3 genes and a quantitative defect of plasmacytoid dendritic cells (pDC), the main cells expressing DNase 1L3, in critical patients. Besides, analysis of public single cell RNAseq data revealed that pDC from COVID-19 patients express less DNase1L3. Conclusion: Severe and critical COVID-19 were associated with an imbalance between NETs and DNase activity with a defect in the amount of DNase 1 and DNase1L3. DNase1L3 deficiency could be explained by a quantitative defect of pDC. Early identification of patients with NETosis imbalance could allow targeted therapies to prevent clinical worsening, such as DNase administration.
dc.language.isoENen_US
dc.subject.enCovid-19
dc.subject.enImmunology
dc.subject.enARDS (Acute Respiratory Distress Syndrome)
dc.title.enBalance between neutrophil extracellular trap formation and DNase activity in COVID-19 patients: a prospective cohort study
dc.typeCommunication dans un congrèsen_US
dc.identifier.doi10.1183/13993003.congress-2023.PA3838en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
bordeaux.pagePA3838en_US
bordeaux.volume62en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - UMR 1219en_US
bordeaux.issuesuppl 67en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.institutionCNRS
bordeaux.conference.titlethe ERS International Congress 2023en_US
bordeaux.countryiten_US
bordeaux.title.proceedingERS International Congress 2023 abstractsen_US
bordeaux.teamGHIGS_BPHen_US
bordeaux.teamELEANOR_BPHen_US
bordeaux.conference.cityMilanen_US
hal.identifierhal-04457539
hal.version1
hal.date.transferred2024-02-14T13:11:01Z
hal.invitednonen_US
hal.proceedingsouien_US
hal.conference.organizerThe European Respiratory Societyen_US
hal.conference.end2023-09-13
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.date=2023-09-09&rft.volume=62&rft.issue=suppl%2067&rft.spage=PA3838&rft.epage=PA3838&rft.eissn=0903-1936&rft.issn=0903-1936&rft.au=PREVEL,%20Renaud&GARCIA,%20GEOFFREY&COLOMER,%20Sylvie&DUVIGNAUD,%20Alexandre&CLEQUIN,%20Etienne&rft.genre=unknown


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