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Patients with COVID-19: in the dark-NETs of neutrophils.

Maximilian AckermannHans-Joachim AndersRostyslav O BilyyGary L BowlinChristoph DanielRebecca De LorenzoMikala EgebladTimo HenneckAndrés HidalgoMarkus H HoffmannBettina HohbergerYogendra KanthiMariana J KaplanJason S KnightJasmin KnopfElzbieta KolaczkowskaPaul KubesMoritz LeppkesAparna MahajanAngelo A ManfrediChristian MaueröderNorma MaugeriIoannis MitroulisLuis Enrique MunozTeluguakula NarasarajuElisabeth NaschbergerIndira NeeliLai Guan NgMarko Z RadicKonstantinos RitisPatrizia Rovere-QueriniMirco SchapherChristine SchauerHans-Uwe SimonJeeshan SinghPanagiotis SkendrosKonstantin StarkMichael StürzlJohan van der VlagPeter VandenabeeleLjubomir VitkovMaren von Köckritz-BlickwedeCansu YanginlarShida YousefiAlexander ZarbockLarissa Valor-MéndezMartin Herrmann
Published in: Cell death and differentiation (2021)
SARS-CoV-2 infection poses a major threat to the lungs and multiple other organs, occasionally causing death. Until effective vaccines are developed to curb the pandemic, it is paramount to define the mechanisms and develop protective therapies to prevent organ dysfunction in patients with COVID-19. Individuals that develop severe manifestations have signs of dysregulated innate and adaptive immune responses. Emerging evidence implicates neutrophils and the disbalance between neutrophil extracellular trap (NET) formation and degradation plays a central role in the pathophysiology of inflammation, coagulopathy, organ damage, and immunothrombosis that characterize severe cases of COVID-19. Here, we discuss the evidence supporting a role for NETs in COVID-19 manifestations and present putative mechanisms, by which NETs promote tissue injury and immunothrombosis. We present therapeutic strategies, which have been successful in the treatment of immunο-inflammatory disorders and which target dysregulated NET formation or degradation, as potential approaches that may benefit patients with severe COVID-19.
Keyphrases
  • coronavirus disease
  • sars cov
  • immune response
  • oxidative stress
  • respiratory syndrome coronavirus
  • early onset
  • toll like receptor
  • drug induced
  • dendritic cells
  • risk assessment
  • combination therapy
  • human health