Impact of the serum of Post-COVID-Syndrome patients without vs with ME/CFS on endothelial cell function

Project description

Background: Peripheral endothelial dysfunction (ED) plays an important role in the pathogenesis of ME/CFS an is characterized by changes in the endothelial cells (EC), which subsequently lead to a reduced vasodilatory response and perfusio. There is also much to suggest the involvement of components of autoimmunity (e.g. autoantibodies). A change in EC functions could be mediated by SARS-CoV-2 infection and could induce the development of autoimmune phenomena in some Post-COVID Syndrome (PCS) patients. In PCS the presence of ME/CFS has been clinically proven (PCS-ME/CFS). In addition, a group of symptomatically similar patients that did not fulfill all ME/CFS criteria have been identified. Our research group found that patients from both groups suffer from ED, but it is still unanswered which cellular mechanisms contribute to this.

Research question:

A) Are there abnormalities in certain serum factors that are related to ED?

B) What influence do the sera of patients vs healthy control subjects have on cultured endothelial cells? Do the two patient groups (PCS and PCS-ME/CFS) differ?

Methods: Sera of Post-COVID Syndrome patients with or without ME/CFS were initially analysed for the presence and quantity of autoantibodies and other bioactive factors. In further experiments, the effect of sera of patients and controls on endothelial cell function in culture was examined.

Results and discussion: Analysis of the effects of patients and controls on EC with regard to their surface markers of release of molecules of activation or damage to the cells

A) No evidence of EC damage or activation by patients sera

B) Different quality and quantity of molecules released by patient sera via the two cohorts (PCS and PCS-ME/CFS)

C) Effects on vessel formation in in vitro culture?

PCS serum mediates an increased formation of vessels. PCS-ME/CFS serum, on the other hand, does not lead to any change in vessel formation compared to the control group. While the observations do not represent a causal explanation for ED, they could be an expression of a lack of compensatory counterregulation in PCS-ME/CFS patients. Factors that promote vessel formation in PCS serum could counteract the already existing ED and vascular dysfunction.

(Description adapted from project website: see link above)