Technology Bundle ID
TAB-1574

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

Applications
Research Materials
Linked ID
E-258-2007-0
Lead Inventors
Philip Murphy (NIAID)
Co-Inventors
Jiliang Gao (NIAID)
Development Status
The technology is a research tool.
ICs
NIAID
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.

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