tetano
Editor, Senior Moderator
Eur J Immunol
. 2022 Oct 14.
doi: 10.1002/eji.202250010. Online ahead of print.
Neutrophil Activation and Neutrophil Extracellular Traps (Nets) in COVID-19 ARDS and Immunothrombosis
Maria Candida Cesta[SUP] 1 [/SUP], Mara Zippoli[SUP] 2 [/SUP], Carolina Marsiglia[SUP] 1 [/SUP], Elizabeth M Gavioli[SUP] 3 [/SUP], Giada Cremonesi[SUP] 4 [/SUP], Akram Khan[SUP] 5 [/SUP], Flavio Mantelli[SUP] 1 [/SUP], Marcello Allegretti[SUP] 1 [/SUP], Robert Balk[SUP] 6 [/SUP]
Affiliations
Abstract
Acute respiratory distress syndrome (ARDS) is an acute inflammatory condition with a dramatic increase in incidence since the beginning of the coronavirus disease 19 (COVID-19) pandemic. Neutrophils play a vital role in the immunopathology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection by triggering the formation of neutrophil extracellular traps (NETs), producing cytokines including interleukin-8 (CXCL8), and mediating the recruitment of other immune cells to regulate processes such as acute and chronic inflammation, which can lead to ARDS. CXCL8 is involved in the recruitment, activation, and degranulation of neutrophils, and therefore contributes to inflammation amplification and severity of disease. Furthermore, activation of neutrophils also supports a prothrombotic phenotype, which may explain the development of immunothrombosis observed in COVID-19 ARDS. This review aims to describe hyperinflammatory ARDS due to SARS-CoV-2 infection. In addition, we address the critical role of polymorphonuclear neutrophils, inflammatory cytokines, and the potential targeting of CXCL8 in treating the hyperinflammatory ARDS population. This article is protected by copyright. All rights reserved.
Keywords: ARDS; COVID-19; CXCL8; cytokine storm; immunomodulators.
. 2022 Oct 14.
doi: 10.1002/eji.202250010. Online ahead of print.
Neutrophil Activation and Neutrophil Extracellular Traps (Nets) in COVID-19 ARDS and Immunothrombosis
Maria Candida Cesta[SUP] 1 [/SUP], Mara Zippoli[SUP] 2 [/SUP], Carolina Marsiglia[SUP] 1 [/SUP], Elizabeth M Gavioli[SUP] 3 [/SUP], Giada Cremonesi[SUP] 4 [/SUP], Akram Khan[SUP] 5 [/SUP], Flavio Mantelli[SUP] 1 [/SUP], Marcello Allegretti[SUP] 1 [/SUP], Robert Balk[SUP] 6 [/SUP]
Affiliations
- PMID: 36239164
- DOI: 10.1002/eji.202250010
Abstract
Acute respiratory distress syndrome (ARDS) is an acute inflammatory condition with a dramatic increase in incidence since the beginning of the coronavirus disease 19 (COVID-19) pandemic. Neutrophils play a vital role in the immunopathology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection by triggering the formation of neutrophil extracellular traps (NETs), producing cytokines including interleukin-8 (CXCL8), and mediating the recruitment of other immune cells to regulate processes such as acute and chronic inflammation, which can lead to ARDS. CXCL8 is involved in the recruitment, activation, and degranulation of neutrophils, and therefore contributes to inflammation amplification and severity of disease. Furthermore, activation of neutrophils also supports a prothrombotic phenotype, which may explain the development of immunothrombosis observed in COVID-19 ARDS. This review aims to describe hyperinflammatory ARDS due to SARS-CoV-2 infection. In addition, we address the critical role of polymorphonuclear neutrophils, inflammatory cytokines, and the potential targeting of CXCL8 in treating the hyperinflammatory ARDS population. This article is protected by copyright. All rights reserved.
Keywords: ARDS; COVID-19; CXCL8; cytokine storm; immunomodulators.