Investigating the Role of Inflammasome Caspases 1 and 11 in the Acute Radiation Syndrome.

Journal Article (Journal Article)

Exposure to high dose radiation causes life-threatening acute and delayed effects. Defining the mechanisms of lethal radiation-induced acute toxicity of gastrointestinal and hematopoietic tissues are critical steps to identify drug targets to mitigate and protect against the acute radiation syndrome (ARS). For example, one rational approach would be to design pharmaceuticals that block cell death pathways to preserve tissue integrity in radiation-sensitive organ systems including the gastrointestinal tract and hematopoietic compartment. A previous study reported that the inflammasome pathway, which mediates inflammatory cell death through pyroptosis, promotes ARS. However, we show that mice lacking the inflammatory executioner caspases, caspase-1 and caspase-11, are not protected from ARS when compared directly to littermates expressing caspase-1 and caspase-11. These results suggest that alternative pathways will need to be targeted by drugs that successfully mitigate and protect against the ARS.

Full Text

Duke Authors

Cited Authors

  • Daniel, AR; Luo, L; Lee, C-L; Kirsch, DG

Published Date

  • December 1, 2021

Published In

Volume / Issue

  • 196 / 6

Start / End Page

  • 686 - 689

PubMed ID

  • 34644390

Pubmed Central ID

  • PMC8665044

Electronic International Standard Serial Number (EISSN)

  • 1938-5404

Digital Object Identifier (DOI)

  • 10.1667/RADE-21-00141.1


  • eng

Conference Location

  • United States