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Immunothrombosis in COVID-19: Implications of Neutrophil Extracellular Traps

SARS-CoV-2 is a member of the family of coronaviruses associated with severe outbreaks of respiratory diseases in recent decades and is the causative agent of the COVID-19 pandemic. The recognition by and activation of the innate immune response recruits neutrophils, which, through their different m...

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Published in:Biomolecules (Basel, Switzerland) Switzerland), 2021-05, Vol.11 (5), p.694
Main Authors: Bautista-Becerril, Brandon, Campi-Caballero, Rebeca, Sevilla-Fuentes, Samuel, Hernández-Regino, Laura M., Hanono, Alejandro, Flores-Bustamante, Al, González-Flores, Julieta, García-Ávila, Carlos A., Aquino-Gálvez, Arnoldo, Castillejos-López, Manuel, Juárez-Cisneros, Armida, Camarena, Angel
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Language:English
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Summary:SARS-CoV-2 is a member of the family of coronaviruses associated with severe outbreaks of respiratory diseases in recent decades and is the causative agent of the COVID-19 pandemic. The recognition by and activation of the innate immune response recruits neutrophils, which, through their different mechanisms of action, form extracellular neutrophil traps, playing a role in infection control and trapping viral, bacterial, and fungal etiological agents. However, in patients with COVID-19, activation at the vascular level, combined with other cells and inflammatory mediators, leads to thrombotic events and disseminated intravascular coagulation, thus leading to a series of clinical manifestations in cerebrovascular, cardiac, pulmonary, and kidney disease while promoting severe disease and mortality. Previous studies of hospitalized patients with COVID-19 have shown that elevated levels of markers specific for NETs, such as free DNA, MPO, and H3Cit, are strongly associated with the total neutrophil count; with acute phase reactants that include CRP, D-dimer, lactate dehydrogenase, and interleukin secretion; and with an increased risk of severe COVID-19. This study analyzed the interactions between NETs and the activation pathways involved in immunothrombotic processes in patients with COVID-19.
ISSN:2218-273X
2218-273X
DOI:10.3390/biom11050694