Neutrophils and Neutrophil Extracellular Traps Drive Necroinflammation in COVID-19.
Angiotensin-Converting Enzyme 2
Animals
Betacoronavirus
/ physiology
COVID-19
Cardiovascular Diseases
/ complications
Coronavirus Infections
/ complications
Diabetes Complications
/ virology
Extracellular Traps
/ immunology
Humans
Inflammation
/ immunology
Necrosis
/ immunology
Neutrophils
/ immunology
Pandemics
Peptidyl-Dipeptidase A
/ metabolism
Pneumonia, Viral
/ complications
SARS-CoV-2
MERS-CoV
NETs
SARS-CoV-2
complement
coronavirus
necroinflammation
neutrophils
thrombosis
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
02 06 2020
02 06 2020
Historique:
received:
06
05
2020
revised:
28
05
2020
accepted:
30
05
2020
entrez:
6
6
2020
pubmed:
6
6
2020
medline:
12
6
2020
Statut:
epublish
Résumé
The COVID-19 pandemic is progressing worldwide with an alarming death toll. There is an urgent need for novel therapeutic strategies to combat potentially fatal complications. Distinctive clinical features of severe COVID-19 include acute respiratory distress syndrome, neutrophilia, and cytokine storm, along with severe inflammatory response syndrome or sepsis. Here, we propose the putative role of enhanced neutrophil infiltration and the release of neutrophil extracellular traps, complement activation and vascular thrombosis during necroinflammation in COVID-19. Furthermore, we discuss how neutrophilic inflammation contributes to the higher mortality of COVID-19 in patients with underlying co-morbidities such as diabetes and cardiovascular diseases. This perspective highlights neutrophils as a putative target for the immunopathologic complications of severely ill COVID-19 patients. Development of the novel therapeutic strategies targeting neutrophils may help reduce the overall disease fatality rate of COVID-19.
Identifiants
pubmed: 32498376
pii: cells9061383
doi: 10.3390/cells9061383
pmc: PMC7348784
pii:
doi:
Substances chimiques
Peptidyl-Dipeptidase A
EC 3.4.15.1
ACE2 protein, human
EC 3.4.17.23
Angiotensin-Converting Enzyme 2
EC 3.4.17.23
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Department of Biotechnology, Ministry of Science and Technology, India
ID : BT/RLF/Re-entry/01/2017
Pays : International
Organisme : Deutsche Forschungsgemeinschaft
ID : AN372/14-3, 23-1, and 24-1
Pays : International
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