Serum of Post-COVID-19 Syndrome patients with or without ME/CFS differentially affects endothelial cell function in vitro
The endothelium is a thin membrane that lines the inside of the heart and blood vessels. Endothelial cells release substances that control vascular relaxation and contraction as well as enzymes that control blood clotting, immune function and platelet (a colorless substance in the blood) adhesion. [Cedars Sinai]
Key points:
- the study was done in vitro i.e. outside the body, often in a test tube
- 3 groups of patients’ blood serum was studied
- both similarities and differences were found in the 2 groups of Post COVID patients (with and without ME/CFS)
- anti-endothelial cell autoantibodies (AECAs) binding to Endothelial cells was significantly increased in Post COVID patients with ME/CFS.
- both differed from healthy controls
Research abstract
Recently, endothelial dysfunction (ED) has been demonstrated in these patients, but the mechanisms remain elusive.
Therefore, we investigated the effects of patients’ sera on endothelia cells (ECs) in vitro. PCS (n = 17), PCS/CFS (n = 13), and healthy controls (HC, n = 14) were screened for serum anti-endothelial cell autoantibodies (AECAs) and dysregulated cytokines.
Serum-treated ECs were analysed for the induction of activation markers and the release of small molecules by flow cytometry. Moreover, the angiogenic potential of sera was measured in a tube formation assay.
While only marginal differences between patient groups were observed for serum cytokines, AECA binding to ECs was significantly increased in PCS/CFS patients.
Surprisingly, PCS and PCS/CFS sera reduced surface levels of several EC activation markers. PCS sera enhanced the release of molecules associated with vascular remodelling and significantly promoted angiogenesis in vitro compared to the PCS/CFS and HC groups.
Angiogenesis – The formation and development of new blood vessels [Wiktionary]
Additionally, sera from both patient cohorts induced the release of molecules involved in inhibition of nitric oxide-mediated endothelial relaxation.
Overall, PCS and PCS/CFS patients′ sera differed in their AECA content and their functional effects on ECs, i.e., secretion profiles and angiogenic potential. We hypothesise a pro-angiogenic effect of PCS sera as a compensatory mechanism to ED which is absent in PCS/CFS patients.
Excerpt from paper:
Based on our observations we speculate on serum factors playing a role in compensatory responses to ED and hypoperfusion in PCS, but not or insufficiently in PCS/CFS patients. Our results may thus provide a new perspective on ME/CFS chronicity which should be further examined.
Authors: Lavinia Flaskamp; Constanze Roubal; Steven Uddin; Franziska Sotzny; Claudia Kedor; Sandra Bauer; Carmen Scheibenbogen; Martina Seifert
Publication: Cells. 2022; 11(15):2376 [doi.org/10.3390/cells11152376] 2 August
