Activation of the NLRP3 inflammasome by particles from the Echinococcus granulosus laminated layer

Cecilia Casaravilla, Álvaro Pittini, Dominik Rückerl, Judith Allen, Álvaro Díaz

Research output: Contribution to journalArticlepeer-review


The interaction of dendritic cells and macrophages with a variety of rigid noncellular particles triggers activation of the NLRP3 inflammasome and consequent secretion of interleukin 1β (IL-1β. Noncellular particles can also be generated in the context of helminth infection, since these large pathogens often shed their outermost structures during growth and/or molting. One such structure is the massive, mucin-based, soft, flexible laminated layer (LL), which protects the larval stages of cestodes of the genus Echinococcus. We show that particles from the Echinococcus granulosus LL (pLL) trigger NLRP3- and caspase-1-dependent IL-1β in lipopolysaccharide (LPS)-primed mouse bone marrow-derived dendritic cells (BMDC). This response can be elicited by pLL too large for phagocytosis and nonetheless requires actin dynamics, Syk, and phosphatidylinositol 3-kinase (PI3K). These three requirements had already been observed in our previous study on the alteration by pLL of CD86, CD40, IL-10, and IL-12 responses to LPS in BMDC; however, we now show that these alterations are independent of NLRP3 and caspase-1. In other words, an initial interaction with particles requiring actin dynamics, Syk, and PI3K, but not phagocytosis, elicits both NLRP3-dependent and NLRP3-independent responses. Intraperitoneal injection of pLL induced IL-1β, suggesting that contact with LL materials induces IL-1β in the E. granulosus infection setting. Our results extend our understanding of NLRP3 inflammasome activation by noncellular particulate materials both to helminth-derived materials and to flexible/soft materials.

Original languageEnglish
Article numbere00190-20
JournalInfection and immunity
Issue number9
Publication statusPublished - Sept 2020


  • Adjuvants
  • Alum
  • Dendritic cells
  • Echinococcus
  • Exophagy
  • Helminths
  • Inflammation
  • Laminated layer
  • Macrophages
  • Membrane affinity-triggered signaling
  • Mucin
  • NLRP3
  • PI3K

Research Beacons, Institutes and Platforms

  • Lydia Becker Institute


Dive into the research topics of 'Activation of the NLRP3 inflammasome by particles from the Echinococcus granulosus laminated layer'. Together they form a unique fingerprint.

Cite this