Mice Genetically Deficient in the Chemoattractant Receptor FPR (formyl peptide receptor)
Description of Invention:
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.
Applications and Modality:
New mouse model to study antibacterial host defense.
Market:
Research tool useful for innate immunity studies.
Development Status:
The technology is a research tool.
Patent Status:
DHHS Reference No. E-258-2007/0 -- Research Tool Patent protection is not being pursued for this technology
Relevant Publication: JL Gao, EJ Lee, PM Murphy. Impaired antibacterial host defense in mice lacking the N-formylpeptide receptor. J Exp Med. 1999 Feb 15;189(4):657-662. [PubMed abs]
Licensing Status: This technology is not patented. The mouse model will be transferred through a Biological Materials License.
Collaborative Research 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.
For Additional Information Please Contact: Peter A. Soukas J.D.
NIH Office of Technology Transfer
6011 Executive Blvd, Suite 325
Rockville, MD 20852-3804
Phone: (301) 435-4646
Email: soukasp@mail.nih.gov
Fax: (301) 402-0220
