ABSTRACT
Background: Patients who have had the disease Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV- 2) COVID-19, mild, moderate or severe, has persisting symptoms weeks to moths after recovery of infection, with the risk of developing long-terms effects. Some alterations are related to damage of the vascular endothelium, generating thrombosis, a direct relation of the endothelial dysfunction. There are not data related on frequency of endothelial colony-forming cells (ECFCs) at 9 months of patients recovered from mild-moderate COVID-19 disease. Aim(s): We analyzed the frequency and morphology of ECFCs from recovered COVID-19 patients at 9 months post-infection. Method(s): Human mononuclear cells (MNCs) were obtained from peripheral blood from 15 recovered COVID-19 patients 9 months after disease, 10 healthy human volunteers with schedule of 2 vaccines (controls 1) and 10 healthy human volunteers without vaccines (controls 2), matched by age. All were men (25-50 years) without a history of major comorbidities. We assayed the frequency, morphological characteristics and proliferation of the ECFCs. The study was approved by the Scientific and Ethical Committee of the IMSS (number IMSS-R- 2020- 785- 167). Informed written consent was obtained from all subjects before enrollment. Result(s): ECFCs were detected in average on day 18 of culture in recovered COVID-19 patients, on day 14 in controls 1 and day 21 in controls 2, respectively. In recovered COVID-19 patients, ECFCs show abnormalities in size with elongations, large cytoplasm with prominent nuclei, similar to senescent state with no proliferative capacity when they were sub-cultured. These findings were different from those observed in controls 1 and 2 respectively. Conclusion(s): We demonstrate for the first time that ECFCs from patients recovered from COVID-19 at 9 months has characteristics of dysfunctional endothelial similar to those observed in patients recovered after 30 days after infection. This finding may support our understanding of the physiology of dysfunctional endothelium from COVID-19 disease at long term.
ABSTRACT
Background: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) named as COVID-19, is associated with damage to the vascular endothelium generating deep vein thrombosis or COVID-19 associated coagulopathy (CAC), a direct relationship with endothelial dysfunction. Vasculitis has been described in biopsies of dead patients and also an increase in circulating endothelial cells (CECs) and their progenitors from patients recovered has been reported. However there are not data focused on frequency, function and morphology in Endothelial Colony Forming Cells (ECFCs). Aims: To investigated the frequency, function and morphology of ECFC from patients recovered from moderate COVID-19 disease. Methods: Human mononuclear cells (MNCs) were obtained from peripheral blood from 15 recovered COVID-19 patients and 10 healthy human volunteers (controls) matched by age, all were men (25-50 years) to obtain ECFCs. We assayed their proliferation and the ability to form capillary-like structures in presence or absence to convalescent plasma of COVID-19 patients. The study protocol was reviewed and approved by the Scientific and Ethical Committee of the IMSS (number IMSS-R-2020-785-167) and according to the guidelines of the 1975 Declaration of Helsinki. Informed written consent was obtained from all subjects before enrollment. Results: ECFCs appeared at 8 and 21 days of culture in recovered COVID-19 patients and controls, respectively. ECFCs increased 3-fold in patients and emerged 1 week earlier. There are differences in the size and the morphology of the colonies of ECFCs from recovered COVID-19 patients, and they were similar to senescent cells. Conclusions: We demonstrate for the first time that ECFCs from patients recovered from COVID-19, present characteristics of dysfunctional endothelial cells that do not have the capacity to carry out angiogenesis processes and to regenerate the vascular endothelium altered by the presence of SARS-CoV-2. This finding may support our understanding of the physiology of dysfunctional endothelium from COVID-19 disease.