Abstract
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.
Highlights
Coronavirus disease 2019 (COVID-19) is an emerging condition caused by the SARSCoV-2 virus, and since December 2019, it has represented a serious public health problem that has compromised health systems worldwide [1]
A SARS-CoV-2 infection triggers an inflammatory response characterized by an increased production of IL-6, IL-8, and IFN-γ and the activation of the nuclear factor enhancing the kappa light chains of activated B cells (NF-kB), jun N-terminal kinase (JNK), and phosphatidylinositol 3-kinase (PI3K) pathways, which are necessary for its permanence [2,11,17,18]
The COVID-19 pandemic has generated a complex scenario for health systems all around the world and has had substantial social and cultural impacts on individuals’ lives
Summary
Coronavirus disease 2019 (COVID-19) is an emerging condition caused by the SARSCoV-2 virus, and since December 2019, it has represented a serious public health problem that has compromised health systems worldwide [1]. Neutrophil extracellular traps (NETs) are structures produced by neutrophils to confine infections These are formed by chromatin meshes, antimicrobial peptides, and enzymes that, when released into the extracellular space, immobilize microorganisms and facilitate their death [5,6,7]. Though beneficial for the host’s defense, the collateral damage from the sustained formation of NETs can trigger a cascade of inflammatory reactions. Such reactions can result in the destruction of surrounding tissues, promote microthrombosis, and cause permanent damage to the organs of the pulmonary and cardiovascular systems, among others [6,7,8]. In this review, the role of NETs as a triggering mechanism for thrombotic processes in patients with COVID-19 is analyzed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
