The mouse Camp gene is an ortholog of the human gene CAMP, which encodes the precursor of cathelicidin antimicrobial peptide LL-37 (or CRAMP in mouse). Expressed mucosal epithelial cells, circulating neutrophils, and myeloid bone marrow cells, Camp is an essential part of the first line of defense against infection. In addition to antimicrobial activity, cathelicidin antimicrobial peptide plays a role in NK cell-mediated tumor growth suppression, and when secreted by neutrophils acts, as an attractant for monocytes, promoting wound healing or angiogenesis. Mouse CRAMP is implicated in adaptive immune response regulation and can interfere with TLR function via interactions with hyaluronan. Mice deficient in CRAMP are more susceptible to experimentally induced necrotic skin infection with Group A Streptococcus, urinary tract infection with uropathogenic E. coli, Pseudomonas aeruginosa infection, and meningococcal Neisseria meningitidis infection.
The Camp (formerly Cnlp) knock-out mice are more susceptible to bacterial infections and may be useful in studies of innate immune response, regulation of immune response, wound healing/angiogenesis and tumor development.
The mice are designated Tangible Research Material (TRM). A complete description, including genotyping, phenotyping, etc is found at The Jackson Lab cat. No. 017799; https://www.jax.org/strain/017799
Academic and non-profit institutions please order directly from The Jackson Laboratory. Commercial entities require a license from UC San Diego contact ( https://innovation.ucsd.edu/contact/).
Cathelicidin LL-37,antimicrobial peptides, innate immunity, immunomodulation, adaptive immunity, neutrophils, inflammation, host defense