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Advances in biological regulation, 2020-08, Vol.77, p.100741-100741, Article 100741
2020
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Autor(en) / Beteiligte
Titel
Devilishly radical NETwork in COVID-19: Oxidative stress, neutrophil extracellular traps (NETs), and T cell suppression
Ist Teil von
  • Advances in biological regulation, 2020-08, Vol.77, p.100741-100741, Article 100741
Ort / Verlag
England: Elsevier Ltd
Erscheinungsjahr
2020
Quelle
MEDLINE
Beschreibungen/Notizen
  • Pandemic coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and poses an unprecedented challenge to healthcare systems due to the lack of a vaccine and specific treatment options. Accordingly, there is an urgent need to understand precisely the pathogenic mechanisms underlying this multifaceted disease. There is increasing evidence that the immune system reacts insufficiently to SARS-CoV-2 and thus contributes to organ damage and to lethality. In this review, we suggest that the overwhelming production of reactive oxygen species (ROS) resulting in oxidative stress is a major cause of local or systemic tissue damage that leads to severe COVID-19. It increases the formation of neutrophil extracellular traps (NETs) and suppresses the adaptive arm of the immune system, i.e. T cells that are necessary to kill virus-infected cells. This creates a vicious cycle that prevents a specific immune response against SARS-CoV-2. The key role of oxidative stress in the pathogenesis of severe COVID-19 implies that therapeutic counterbalancing of ROS by antioxidants such as vitamin C or NAC and/or by antagonizing ROS production by cells of the mononuclear phagocyte system (MPS) and neutrophil granulocytes and/or by blocking of TNF-α can prevent COVID-19 from becoming severe. Controlled clinical trials and preclinical models of COVID-19 are needed to evaluate this hypothesis.
Sprache
Englisch
Identifikatoren
ISSN: 2212-4926
eISSN: 2212-4934
DOI: 10.1016/j.jbior.2020.100741
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7334659
Format
Schlagworte
Acetylcysteine - therapeutic use, Adaptive systems, Antioxidants, Antioxidants - therapeutic use, Ascorbic acid, Ascorbic Acid - therapeutic use, Betacoronavirus - immunology, Betacoronavirus - pathogenicity, Clinical trials, Coronaviridae, Coronavirus Infections - drug therapy, Coronavirus Infections - epidemiology, Coronavirus Infections - immunology, Coronavirus Infections - virology, Coronaviruses, COVID-19, Cytokines - genetics, Cytokines - immunology, Damage, Extracellular Traps - drug effects, Extracellular Traps - immunology, Extracellular Traps - metabolism, Host-Pathogen Interactions - drug effects, Host-Pathogen Interactions - genetics, Host-Pathogen Interactions - immunology, Humans, Immune response, Immune system, Immunity, Innate - drug effects, Lethality, Leukocytes (granulocytic), Lymphocytes, Lymphocytes T, Lymphopenia, Lymphopenia - drug therapy, Lymphopenia - epidemiology, Lymphopenia - immunology, Lymphopenia - virology, Mononuclear phagocyte system, Neutrophil extracellular traps (NETs), Neutrophils, Neutrophils - drug effects, Neutrophils - immunology, Neutrophils - virology, NF-kappa B - genetics, NF-kappa B - immunology, Oxidative stress, Oxidative Stress - drug effects, Pandemics, Pathogenesis, Pneumonia, Viral - drug therapy, Pneumonia, Viral - epidemiology, Pneumonia, Viral - immunology, Pneumonia, Viral - virology, Reactive oxygen species, Reactive Oxygen Species - antagonists & inhibitors, Reactive Oxygen Species - immunology, Reactive Oxygen Species - metabolism, Respiratory diseases, SARS-CoV-2, Severe acute respiratory syndrome, Severe acute respiratory syndrome coronavirus 2, T cells, T-Lymphocytes - drug effects, T-Lymphocytes - immunology, T-Lymphocytes - virology, Tumor necrosis factor-α, Vaccines, Viral diseases, Viruses

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