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Markers of endothelial cell activation are associated with the severity of pulmonary disease in COVID-19.
Osburn, William O; Smith, Kimberly; Yanek, Lisa; Amat-Alcaron, Nuria; Thiemann, David R; Cox, Andrea L; Leucker, Thorsten M; Lowenstein, Charles J.
  • Osburn WO; Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
  • Smith K; Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
  • Yanek L; Division of General Internal Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
  • Amat-Alcaron N; Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
  • Thiemann DR; Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
  • Cox AL; Division of Infectious Diseases, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
  • Leucker TM; Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
  • Lowenstein CJ; Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States of America.
PLoS One ; 17(5): e0268296, 2022.
Article in English | MEDLINE | ID: covidwho-1910641
ABSTRACT
Severe coronavirus disease-19 (COVID-19) is characterized by vascular inflammation and thrombosis. We and others have proposed that the inflammatory response to coronavirus infection activates endothelial cells, leading to endothelial release of pro-thrombotic proteins. These mediators can trigger obstruction of the pulmonary microvasculature, leading to worsening oxygenation, acute respiratory distress syndrome, and death. In the current study, we tested the hypothesis that higher levels of biomarkers released from endothelial cells are associated with worse oxygenation in patients with COVID-19. We studied 83 participants aged 18-84 years with COVID-19 admitted to a single center. The severity of pulmonary disease was classified by oxygen requirement, including no oxygen requirement, low-flow oxygen, high-flow nasal cannula oxygen, mechanical ventilation, and death. We measured plasma levels of two proteins released by activated endothelial cells, von Willebrand Factor (VWF) antigen and soluble P-Selectin (sP-Sel), and a biomarker of systemic thrombosis, D-dimer. Additionally, we explored the association of endothelial biomarker levels with the levels of pro-inflammatory cytokine and chemokines, and vascular inflammation biomarkers. We found that levels of VWF, sP-sel, and D-dimer were increased in individuals with more severe COVID-19 pulmonary disease. Biomarkers of endothelial cell activation were also correlated with proinflammatory cytokines and chemokines. Taken together, our data demonstrate increased levels of VWF and sP-selectin are linked to the severity of lung disease in COVID-19 and correlated with biomarkers of inflammation and vascular inflammation. Our data support the concept that COVID-19 is a vascular disease which involves endothelial injury in the context of an inflammatory state.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Thrombosis / COVID-19 Type of study: Prognostic study Topics: Variants Limits: Humans Language: English Journal: PLoS One Journal subject: Science / Medicine Year: 2022 Document Type: Article Affiliation country: Journal.pone.0268296

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Thrombosis / COVID-19 Type of study: Prognostic study Topics: Variants Limits: Humans Language: English Journal: PLoS One Journal subject: Science / Medicine Year: 2022 Document Type: Article Affiliation country: Journal.pone.0268296