Interleukin-1 and the NLRP3 inflammasome in COVID-19: Pathogenetic and therapeutic implications: IL-1 and NLRP3 inflammasome in COVID-19

Nicola Potere, Marco Giuseppe Del Buono, Roberto Caricchio, Paul C. Cremer, Alessandra Vecchié, Ettore Porreca, Daniela Dalla Gasperina, Francesco Dentali, Antonio Abbate, Aldo Bonaventura*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

44 Scopus citations

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-1β (IL-1β) 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-1β in COVID-19, and discuss clinical trials testing IL-1 inhibition in COVID-19.

Original languageEnglish (US)
Article number104299
JournalEBioMedicine
Volume85
DOIs
StatePublished - Nov 2022

Keywords

  • Anakinra
  • C-reactive protein
  • Canakinumab
  • Colchicine
  • COVID-19
  • IL-18
  • IL-1β
  • NLRP3 inflammasome
  • SARS-CoV-2

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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