Endothelial dysfunction contributes to severe COVID-19 in combination with dysregulated lymphocyte responses and cytokine networks

dc.contributor.authorRuhl, Louisa
dc.contributor.authorPink, Isabell
dc.contributor.authorKühne, Jenny F.
dc.contributor.authorBeushausen, Kerstin
dc.contributor.authorKeil, Jana
dc.contributor.authorChristoph, Stella
dc.contributor.authorSauer, Andrea
dc.contributor.authorBoblitz, Lennart
dc.contributor.authorSchmidt, Julius
dc.contributor.authorDavid, Sascha
dc.contributor.authorJäck, Hans-Martin
dc.contributor.authorRoth, Edith
dc.contributor.authorCornberg, Markus
dc.contributor.authorSchulz, Thomas F.
dc.contributor.authorWelte, Tobias
dc.contributor.authorHöper, Marius M.
dc.contributor.authorFalk, Christine S.
dc.date.accessioned2023-03-28
dc.date.available2023-10-09T20:21:30Z
dc.date.created2021
dc.date.issued2023-03-28
dc.description.abstractThe systemic processes involved in the manifestation of life-threatening COVID-19 and in disease recovery are still incompletely understood, despite investigations focusing on the dysregulation of immune responses after SARS-CoV-2 infection. To define hallmarks of severe COVID-19 in acute disease (n = 58) and in disease recovery in convalescent patients (n = 28) from Hannover Medical School, we used flow cytometry and proteomics data with unsupervised clustering analyses. In our observational study, we combined analyses of immune cells and cytokine/chemokine networks with endothelial activation and injury. ICU patients displayed an altered immune signature with prolonged lymphopenia but the expansion of granulocytes and plasmablasts along with activated and terminally differentiated T and NK cells and high levels of SARS-CoV-2-specific antibodies. The core signature of seven plasma proteins revealed a highly inflammatory microenvironment in addition to endothelial injury in severe COVID-19. Changes within this signature were associated with either disease progression or recovery. In summary, our data suggest that besides a strong inflammatory response, severe COVID-19 is driven by endothelial activation and barrier disruption, whereby recovery depends on the regeneration of the endothelial integrity.en
dc.identifier.citationSignal Transduction and Targeted Therapy 6 (2021): 418. <https://www.nature.com/articles/s41392-021-00819-6>
dc.identifier.doihttps://doi.org/10.1038/s41392-021-00819-6
dc.identifier.issn2059-3635
dc.identifier.opus-id22474
dc.identifier.urihttps://open.fau.de/handle/openfau/22474
dc.identifier.urnurn:nbn:de:bvb:29-opus4-224748
dc.language.isoen
dc.publisherNature Publishing Group UK
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.de
dc.subjectAdaptive immunity
dc.subjectInfectious diseases
dc.subject.ddcDDC Classification::6 Technik, Medizin, angewandte Wissenschaften :: 61 Medizin und Gesundheit :: 610 Medizin und Gesundheit
dc.titleEndothelial dysfunction contributes to severe COVID-19 in combination with dysregulated lymphocyte responses and cytokine networksen
dc.typearticle
dcterms.publisherFriedrich-Alexander-Universität Erlangen-Nürnberg (FAU)
local.date.prevpublished2021-12-10
local.document.articlenumber418
local.journal.issue1
local.journal.titleSignal Transduction and Targeted Therapy
local.journal.volume6
local.sendToDnbfree*
local.subject.fakultaetMedizinische Fakultät
local.subject.importimport
local.subject.sammlungUniversität Erlangen-Nürnberg / Eingespielte Open Access Artikel / Eingespielte Open Access Artikel 2023
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