The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response

  • Alberto Baroja-Mazo
  • , Fatima Martín-Sánchez
  • , Ana I. Gomez
  • , Carlos M. Martínez
  • , Joaquín Amores-Iniesta
  • , Vincent Compan
  • , Maria Barberà-Cremades
  • , Jordi Yagüe
  • , Estibaliz Ruiz-Ortiz
  • , Jordi Antón
  • , Segundo Buján
  • , Isabelle Couillin
  • , David Brough
  • , Juan I. Arostegui
  • , Pablo Pelegrín

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Assembly of the NLRP3 inflammasome activates caspase-1 and mediates the processing and release of the leaderless cytokine IL-1β and thereby serves a central role in the inflammatory response and in diverse human diseases. Here we found that upon activation of caspase-1, oligomeric NLRP3 inflammasome particles were released from macrophages. Recombinant oligomeric protein particles composed of the adaptor ASC or the p.D303N mutant form of NLRP3 associated with cryopyrin-associated periodic syndromes (CAPS) stimulated further activation of caspase-1 extracellularly, as well as intracellularly after phagocytosis by surrounding macrophages. We found oligomeric ASC particles in the serum of patients with active CAPS but not in that of patients with other inherited autoinflammatory diseases. Our findings support a model whereby the NLRP3 inflammasome, acting as an extracellular oligomeric complex, amplifies the inflammatory response. © 2014 Nature America, Inc. All rights reserved.
    Original languageEnglish
    Pages (from-to)738-748
    Number of pages10
    JournalNature Immunology
    Volume15
    Issue number8
    DOIs
    Publication statusPublished - 22 Jun 2014

    Research Beacons, Institutes and Platforms

    • Dementia@Manchester

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