Adipose triglyceride lipase suppresses noncanonical inflammasome by hydrolyzing LPS

Nat Chem Biol. 2024 Nov;20(11):1434-1442. doi: 10.1038/s41589-024-01569-6. Epub 2024 Feb 27.

Abstract

Intracellular recognition of lipopolysaccharide (LPS) by mouse caspase-11 or human caspase-4 is a vital event for the activation of the noncanonical inflammasome. Whether negative regulators are involved in intracellular LPS sensing is still elusive. Here we show that adipose triglyceride lipase (ATGL) is a negative regulator of the noncanonical inflammasome. Through screening for genes participating in the noncanonical inflammasome, ATGL is identified as a negative player for intracellular LPS signaling. ATGL binds LPS and catalyzes the removal of the acylated side chains that contain ester bonds. LPS with under-acylated side chains no longer activates the inflammatory caspases. Cells with ATGL deficiency exhibit enhanced immune responses when encountering intracellular LPS, including an elevated secretion of interleukin-1β, decreased cell viability and increased cell cytotoxicity. Moreover, ATGL-deficient mice show exacerbated responses to endotoxin challenges. Our results uncover that ATGL degrades cytosolic LPS to suppress noncanonical inflammasome activation.

MeSH terms

  • Animals
  • Caspases, Initiator / metabolism
  • Cell Survival / drug effects
  • Humans
  • Hydrolysis
  • Inflammasomes* / metabolism
  • Interleukin-1beta / metabolism
  • Lipase* / genetics
  • Lipase* / metabolism
  • Lipopolysaccharides* / pharmacology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout

Substances

  • Casp4 protein, mouse
  • Caspases, Initiator
  • Inflammasomes
  • Interleukin-1beta
  • Lipase
  • Lipopolysaccharides
  • PNPLA2 protein, mouse
  • PNPLA2 protein, human