Interleukin-1 and the NLRP3 inflammasome in COVID-19: Pathogenetic and therapeutic implications.
EBioMedicine
; 85: 104299, 2022 Nov.
Article
in English
| MEDLINE | ID: covidwho-2061075
ABSTRACT
A hyperinflammatory response during severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection crucially worsens clinical evolution of coronavirus disease 2019 (COVID-19). The interaction between SARS-CoV-2 and angiotensin-converting enzyme 2 (ACE2) triggers the activation of the NACHT, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome. Enhanced inflammasome activity has been associated with increased disease severity and poor prognosis. Evidence suggests that inflammasome activation and interleukin-1ß (IL-1ß) release aggravate pulmonary injury and induce hypercoagulability, favoring progression to respiratory failure and widespread thrombosis eventually leading to multiorgan failure and death. Observational studies with the IL-1 blockers anakinra and canakinumab provided promising results. In the SAVE-MORE trial, early treatment with anakinra significantly shortened hospital stay and improved survival in patients with moderate-to-severe COVID-19. In this review, we summarize current evidence supporting the pathogenetic role of the NLRP3 inflammasome and IL-1ß in COVID-19, and discuss clinical trials testing IL-1 inhibition in COVID-19.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Inflammasomes
/
COVID-19
/
COVID-19 Drug Treatment
Type of study:
Observational study
/
Prognostic study
/
Randomized controlled trials
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
EBioMedicine
Year:
2022
Document Type:
Article
Affiliation country:
J.ebiom.2022.104299
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