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


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.

Potential Commercial Applications: Competitive Advantages:
  • FPR knock out mouse can be used as antibacterial host defense model and innate immunity studies.
 


Development Stage:
The technology is a research tool.

Inventors:

Philip Murphy (NIAID)  ➽ more inventions...

Jiliang Gao (NIAID)  ➽ more inventions...


Intellectual Property:
Research Tool -- Patent protection is not being pursued for this technology. (IC Reference No. 2007-087)

Publications:
Gao JL, et al. PMID 9989980

Collaboration Opportunity:

The Laboratory of Molecular Immunology, NIAID, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize FPR knockout mice. Please contact Philip Murphy, M.D. at Tel: 301-496-8616 and/or pmm@nih.gov for more information.


Licensing Contact:
Charles Rainwater,
Email: crainwater@niaid.nih.gov
Phone: 301-496-2644

OTT Reference No: E-258-2007/0
Updated: Sep 19, 2017