Revisão Acesso aberto Revisado por pares

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

2021; Springer Nature; Volume: 28; Issue: 11 Linguagem: Inglês

10.1038/s41418-021-00805-z

ISSN

1476-5403

Autores

Maximilian Ackermann, Hans‐Joachim Anders, Rostyslav Bilyy, Gary L. Bowlin, Christoph Daniel, Rebecca De Lorenzo, Mikala Egeblad, Timo Henneck, Andrés Hidalgo, Markus Hoffmann, Bettina Hohberger, Yogendra Kanthi, Mariana J. Kaplan, Jason S. Knight, Jasmin Knopf, Elżbieta Kołaczkowska, Paul Kubes, Moritz Leppkes, Aparna Mahajan, Angelo A. Manfredi, Christian Maueröder, Norma Maugeri, Ioannis Mitroulis, Luis E. Muñoz, Teluguakula Narasaraju, Elisabeth Naschberger, Indira Neeli, Lai Guan Ng, Marko Radic, Konstantinos Ritis, Patrizia Rovere‐Querini, Mirco Schapher, Christine Schauer, Hans‐Uwe Simon, Jeeshan Singh, Panagiotis Skendros, Konstantin Stark, Michael Stürzl, Johan van der Vlag, Peter Vandenabeele, Ljubomir Vitkov, Maren von Köckritz‐Blickwede, Cansu Yanginlar, Shída Yousefi, Alexander Zarbock, Georg Schett, Martin Herrmann,

Tópico(s)

Inflammasome and immune disorders

Resumo

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.

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