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suck abstract from ncbi


10.1038/s41392-021-00819-6

http://scihub22266oqcxt.onion/10.1038/s41392-021-00819-6
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suck abstract from ncbi


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pmid34893580      Signal+Transduct+Target+Ther 2021 ; 6 (1): 418
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  • Endothelial dysfunction contributes to severe COVID-19 in combination with dysregulated lymphocyte responses and cytokine networks #MMPMID34893580
  • Ruhl L; Pink I; Kuhne JF; Beushausen K; Keil J; Christoph S; Sauer A; Boblitz L; Schmidt J; David S; Jack HM; Roth E; Cornberg M; Schulz TF; Welte T; Hoper MM; Falk CS
  • Signal Transduct Target Ther 2021[Dec]; 6 (1): 418 PMID34893580show ga
  • The 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.
  • |Antibodies, Viral/*blood[MESH]
  • |Biomarkers/blood[MESH]
  • |Blood Proteins/*metabolism[MESH]
  • |C-Reactive Protein/metabolism[MESH]
  • |COVID-19/*diagnosis/immunology/mortality/virology[MESH]
  • |Chemokine CXCL10/blood[MESH]
  • |Chemokine CXCL9/blood[MESH]
  • |Cluster Analysis[MESH]
  • |Convalescence[MESH]
  • |Cytokine Release Syndrome/*diagnosis/immunology/mortality/virology[MESH]
  • |Disease Progression[MESH]
  • |Endothelium, Vascular/immunology/*virology[MESH]
  • |Granulocytes/immunology/virology[MESH]
  • |Hematopoietic Cell Growth Factors/blood[MESH]
  • |Hepatocyte Growth Factor/blood[MESH]
  • |Humans[MESH]
  • |Intensive Care Units[MESH]
  • |Interleukin-12 Subunit p40/blood[MESH]
  • |Interleukin-6/blood[MESH]
  • |Interleukin-8/blood[MESH]
  • |Killer Cells, Natural/immunology/virology[MESH]
  • |Lectins, C-Type/blood[MESH]
  • |Lymphopenia/*diagnosis/immunology/mortality/virology[MESH]
  • |Plasma Cells/immunology/virology[MESH]
  • |SARS-CoV-2/*pathogenicity[MESH]
  • |Survival Analysis[MESH]


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