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Winkler MS, Claus RA, Schilder M, et al. Erythrocytes increase endogenous sphingosine 1-phosphate levels as an adaptive response to SARS-CoV-2 infection. Clin Sci (Lond). 2021;135(24):2781-2791doi: 10.1042/CS20210666.
Winkler, M. S., Claus, R. A., Schilder, M., Pöhlmann, S., Coldewey, S. M., Grundmann, J., Fricke, T., Moerer, O., Meissner, K., Bauer, M., Hofmann-Winkler, H., & Gräler, M. H. (2021). Erythrocytes increase endogenous sphingosine 1-phosphate levels as an adaptive response to SARS-CoV-2 infection. Clinical science (London, England : 1979), 135(24), 2781-2791. https://doi.org/10.1042/CS20210666
Winkler, Martin Sebastian, et al. "Erythrocytes increase endogenous sphingosine 1-phosphate levels as an adaptive response to SARS-CoV-2 infection." Clinical science (London, England : 1979) vol. 135,24 (2021): 2781-2791. doi: https://doi.org/10.1042/CS20210666
Winkler MS, Claus RA, Schilder M, Pöhlmann S, Coldewey SM, Grundmann J, Fricke T, Moerer O, Meissner K, Bauer M, Hofmann-Winkler H, Gräler MH. Erythrocytes increase endogenous sphingosine 1-phosphate levels as an adaptive response to SARS-CoV-2 infection. Clin Sci (Lond). 2021 Dec 22;135(24):2781-2791. doi: 10.1042/CS20210666. PMID: 34878105.
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Clin Sci (Lond). 2021 Dec 22;135(24):2781-2791. doi: 10.1042/CS20210666.

Erythrocytes increase endogenous sphingosine 1-phosphate levels as an adaptive response to SARS-CoV-2 infection.

Clinical science (London, England : 1979)

Martin Sebastian Winkler, Ralf Alexander Claus, Mareike Schilder, Stefan Pöhlmann, Sina M Coldewey, Julian Grundmann, Torben Fricke, Onnen Moerer, Konrad Meissner, Michael Bauer, Heike Hofmann-Winkler, Markus H Gräler

Affiliations

  1. Department of Anesthesiology, Emergency and Intensive Care Medicine, University of Göttingen, Göttingen, Germany.
  2. Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
  3. Center for Molecular Biomedicine (CMB), Jena University Hospital, Jena, Germany.
  4. Infection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, Göttingen, Germany.
  5. Faculty of Biology and Psychology, University Göttingen, Göttingen, Germany.
  6. Center for Sepsis Control and Care (CSCC), Jena University Hospital, Jena, Germany.
  7. Septomics Research Center, Jena University Hospital, Jena, Germany.

PMID: 34878105 DOI: 10.1042/CS20210666

Abstract

Low plasma levels of the signaling lipid metabolite sphingosine 1-phosphate (S1P) are associated with disrupted endothelial cell (EC) barriers, lymphopenia and reduced responsivity to hypoxia. Total S1P levels were also reduced in 23 critically ill patients with coronavirus disease 2019 (COVID-19), and the two main S1P carriers, serum albumin (SA) and high-density lipoprotein (HDL) were dramatically low. Surprisingly, we observed a carrier-changing shift from SA to HDL, which probably prevented an even further drop in S1P levels. Furthermore, intracellular S1P levels in red blood cells (RBCs) were significantly increased in COVID-19 patients compared with healthy controls due to up-regulation of S1P producing sphingosine kinase 1 and down-regulation of S1P degrading lyase expression. Cell culture experiments supported increased sphingosine kinase activity and unchanged S1P release from RBC stores of COVID-19 patients. These observations suggest adaptive mechanisms for maintenance of the vasculature and immunity as well as prevention of tissue hypoxia in COVID-19 patients.

© 2021 The Author(s).

Keywords: SARS-CoV-2; endothelial cell barrier; erythrocytes; high-density lipoprotein; hypoxia; infection

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