Technology ID

Mice Genetically Deficient in the Chemoattractant Receptor FPR (formyl peptide receptor)

Lead Inventor
Murphy, Philip (NIAID)
Gao, Jiliang (NIAID)
Research Materials
Consumer Products
Therapeutic Areas
Infectious Disease
Development Status
The technology is a research tool.
Research Products
Animal Models
Lead IC
The present research tool is a knockout mouse model (FPR-/-) that lacks the high affinity N-formylpeptide receptor (FPR), created by targeted gene disruption.

N-formylpeptides derive from bacterial and mitochondrial proteins, and bind to specific receptors on mammalian phagocytes. Since binding induces chemotaxis and activation of phagocytes in vitro, it has been postulated that N-formylpeptide receptor signaling in vivo may be important in antibacterial host defense, although direct proof has been lacking. The inventors have found that FPR-/- mice have no obvious developmental defects and do not develop spontaneous infection when derived in specific pathogen-free conditions. This suggests that, under these conditions, FPR is dispensable. However, when challenged with L. monocytogenes, FPR-deficient mice have accelerated mortality and increased bacterial burden in liver and spleen early after infection, which suggests a role for FPR in host defense, specifically through regulation of innate immunity.
Commercial Applications
  • FPR knock out mouse can be used as antibacterial host defense model and innate immunity studies.
Licensing Contact:
Rainwater, Charles