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Tissue damage from neutrophil-induced oxidative stress in COVID-19
by
Massaad Charbel
, Nuss, Philippe
, Laforge Mireille
, Elbim Carole
, Benoliel Jean-Jacques
, Hémadi Miryana
, Becker, Chrystel
, Frère Corinne
in
Coronaviruses
/ COVID-19
/ Erythrocytes
/ Leukocytes (neutrophilic)
/ Lymphocytes
/ Neutrophils
/ Oxidative stress
/ Reactive oxygen species
/ Thromboembolism
/ Thrombosis
2020
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Tissue damage from neutrophil-induced oxidative stress in COVID-19
by
Massaad Charbel
, Nuss, Philippe
, Laforge Mireille
, Elbim Carole
, Benoliel Jean-Jacques
, Hémadi Miryana
, Becker, Chrystel
, Frère Corinne
in
Coronaviruses
/ COVID-19
/ Erythrocytes
/ Leukocytes (neutrophilic)
/ Lymphocytes
/ Neutrophils
/ Oxidative stress
/ Reactive oxygen species
/ Thromboembolism
/ Thrombosis
2020
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Do you wish to request the book?
Tissue damage from neutrophil-induced oxidative stress in COVID-19
by
Massaad Charbel
, Nuss, Philippe
, Laforge Mireille
, Elbim Carole
, Benoliel Jean-Jacques
, Hémadi Miryana
, Becker, Chrystel
, Frère Corinne
in
Coronaviruses
/ COVID-19
/ Erythrocytes
/ Leukocytes (neutrophilic)
/ Lymphocytes
/ Neutrophils
/ Oxidative stress
/ Reactive oxygen species
/ Thromboembolism
/ Thrombosis
2020
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Tissue damage from neutrophil-induced oxidative stress in COVID-19
Journal Article
Tissue damage from neutrophil-induced oxidative stress in COVID-19
2020
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Overview
The high neutrophil to lymphocyte ratio observed in critically ill patients with COVID-19 is associated with excessive levels of reactive oxygen species (ROS), which promote a cascade of biological events that drive pathological host responses. ROS induce tissue damage, thrombosis and red blood cell dysfunction, which contribute to COVID-19 disease severity. We suggest that free radical scavengers could be beneficial for the most vulnerable patients.In this Comment article, Becker and colleagues consider how the excessive release of reactive oxygen species by neutrophils may perpetuate red blood cell dysfunction, thrombosis and tissue damage in severe cases of COVID-19.
Publisher
Nature Publishing Group
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