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Review
. 2022 Mar 11:13:821007.
doi: 10.3389/fimmu.2022.821007. eCollection 2022.

On the Origin of Neutrophil Extracellular Traps in COVID-19

Michal Pastorek  1 , Martin Dúbrava  2 , Peter Celec  1   3   4
Affiliations
Review

On the Origin of Neutrophil Extracellular Traps in COVID-19

Michal Pastorek et al. Front Immunol. .

Abstract

Despite ongoing vaccination COVID-19 is a global healthcare problem because of the lack of an effective _targeted therapy. In severe COVID-19 manifesting as acute respiratory distress syndrome, uncontrolled innate immune system activation results in cytokine deregulation, damage-associated molecular patterns release upon tissue damage and high occurrence of thrombotic events. These pathomechanisms are linked to neutrophil function and dysfunction, particularly increased formation of neutrophil extracellular traps (NETs). While the association of NETs and severity of COVID-19 has been shown and proved, the causes of NETs formation are unclear. The aim of this review is to summarize potential inducers of NETs formation in severe COVID-19 and to discuss potential treatment options _targeting NETs formation of removal.

Keywords: COVID – 19; DAMPs; extracellular traps (ETs); neutrophil; thrombosis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Potential mechanism underlying NETs formation and thrombosis induction in COVID-19. Upon SARS-CoV-2 infection, pneumocyte death and endothelial dysfunction result in the release of DAMPs and SARS-CoV-2 into extracellular space, where they bind to PRRs and ACE2 receptors and initiate activation of neutrophils and formation of NETs. NETs that are not removed from the circulation induce more NETs in a vicious circle and cause thrombosis and inflammation that might even lead to cytokine storm. Additionally, binding of SARS-CoV-2 on ACE2 receptor of endothelial cells may promote angiotensin II and angiotensin 1-7 imbalance leading to endothelial dysfunction and inflammation, which further contributes to NETs induction and thrombus formation. Figure was created with BioRender.com.
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