Bibliographic Details
| Title: |
The efficacy of therapeutic plasma exchange in COVID-19 patients on endothelial tightness in vitro is hindered by platelet activation |
| Authors: |
Theo Ebermeyer, Olivier Hequet, Frederic Berard, Amelie Prier, Marie-Ange Eyraud, Charles-Antoine Arthaud, Marco Heestermans, Anne-Claire Duchez, Aurelie Guironnet-Paquet, Philippe Berthelot, Fabrice Cognasse, Hind Hamzeh-Cognasse |
| Source: |
Frontiers in Cardiovascular Medicine, Vol 10 (2023) |
| Publisher Information: |
Frontiers Media S.A., 2023. |
| Publication Year: |
2023 |
| Collection: |
LCC:Diseases of the circulatory (Cardiovascular) system |
| Subject Terms: |
COVID-19, therapeutic plasma exchange, endothelium, platelet, inflammation, Diseases of the circulatory (Cardiovascular) system, RC666-701 |
| More Details: |
Coronavirus disease (COVID)-19 is characterised in particular by vascular inflammation with platelet activation and endothelial dysfunction. During the pandemic, therapeutic plasma exchange (TPE) was used to reduce the cytokine storm in the circulation and delay or prevent ICU admissions. This procedure consists in replacing the inflammatory plasma by fresh frozen plasma from healthy donors and is often used to remove pathogenic molecules from plasma (autoantibodies, immune complexes, toxins, etc.). This study uses an in vitro model of platelet-endothelial cell interactions to assess changes in these interactions by plasma from COVID-19 patients and to determine the extent to which TPE reduces such changes. We noted that exposure of an endothelial monolayer to plasmas from COVID-19 patients post-TPE induced less endothelial permeability compared to COVID-19 control plasmas. Yet, when endothelial cells were co-cultured with healthy platelets and exposed to the plasma, the beneficial effect of TPE on endothelial permeability was somewhat reduced. This was linked to platelet and endothelial phenotypical activation but not with inflammatory molecule secretion. Our work shows that, in parallel to the beneficial removal of inflammatory factors from the circulation, TPE triggers cellular activation which may partly explain the reduction in efficacy in terms of endothelial dysfunction. These findings provide new insights for improving the efficacy of TPE using supporting treatments targeting platelet activation, for instance. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2297-055X |
| Relation: |
https://www.frontiersin.org/articles/10.3389/fcvm.2023.1094786/full; https://doaj.org/toc/2297-055X |
| DOI: |
10.3389/fcvm.2023.1094786 |
| Access URL: |
https://doaj.org/article/79a628cff13843e8889c85f039eb9378 |
| Accession Number: |
edsdoj.79a628cff13843e8889c85f039eb9378 |
| Database: |
Directory of Open Access Journals |
