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Transfus Apher Sci ; 60(6): 103237, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1366698


SARS-CoV-2 attaches to the angiotensin-converting enzyme 2 (ACE-2) receptor on human cells. The virus causes hypercytokinemia, capillary leak, pulmonary edema, acute respiratory distress syndrome, acute cardiac injury, and leads to death. Mesenchymal stem cells (MSCs) are ACE-2 negative cells; therefore, can escape from SARS-CoV-2. MSCs prevent hypercytokinemia and help the resolution of the pulmonary edema and other damages occurred during the course of COVID-19. In addition, MSCs enhance the regeneration of the lung and other tissues affected by SARS-CoV-2. The case series reported beneficial effect of MSCs in COVID-19 treatment. However, there are some concerns about the safety of MSCs, particularly referring to the increased risk of disseminated intravascular coagulation, and thromboembolism due to the expression of TF/CD142. Prospective, randomized, large scale studies are needed to reveal the optimum dose, administration way, time, efficacy, and safety of MSCs in the COVID-19 treatment.

COVID-19 , Lung/physiology , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/metabolism , Regeneration , SARS-CoV-2/metabolism , COVID-19/blood , COVID-19/epidemiology , COVID-19/therapy , Disseminated Intravascular Coagulation/blood , Disseminated Intravascular Coagulation/etiology , Humans , Peptidyl-Dipeptidase A/metabolism , Prospective Studies , Risk Factors , Thromboembolism/blood , Thromboembolism/etiology , Thromboplastin/biosynthesis
J Clin Invest ; 130(11): 5674-5676, 2020 11 02.
Article in English | MEDLINE | ID: covidwho-760323


In a stunningly short period of time, the unexpected coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has turned the unprepared world topsy-turvy. Although the rapidity with which the virus struck was indeed overwhelming, scientists throughout the world have been up to the task of deciphering the mechanisms by which SARS-CoV-2 induces the multisystem and multiorgan inflammatory responses that, collectively, contribute to the high mortality rate in affected individuals. In this issue of the JCI, Skendros and Mitsios et al. is one such team who report that the complement system plays a substantial role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to the severity of COVID-19. In support of the hypothesis that the complement system along with neutrophils and platelets contributes to COVID-19, the authors present empirical evidence showing that treatment with the complement inhibitor compstatin Cp40 inhibited the expression of tissue factor in neutrophils. These results confirm that the complement axis plays a critical role and suggest that targeted therapy using complement inhibitors is a potential therapeutic option to treat COVID-19-induced inflammation.

Betacoronavirus/metabolism , Complement Activation/drug effects , Coronavirus Infections , Pandemics , Peptides, Cyclic/pharmacology , Pneumonia, Viral , Thromboplastin/biosynthesis , Thrombotic Microangiopathies , Blood Platelets/metabolism , Blood Platelets/pathology , COVID-19 , Coronavirus Infections/drug therapy , Coronavirus Infections/metabolism , Coronavirus Infections/pathology , Humans , Inflammation/drug therapy , Inflammation/metabolism , Inflammation/pathology , Inflammation/virology , Neutrophils/metabolism , Neutrophils/pathology , Pneumonia, Viral/drug therapy , Pneumonia, Viral/metabolism , Pneumonia, Viral/pathology , SARS-CoV-2 , Severity of Illness Index , Thrombotic Microangiopathies/drug therapy , Thrombotic Microangiopathies/metabolism , Thrombotic Microangiopathies/pathology , Thrombotic Microangiopathies/virology