Nmur1 −/− mice are not protected from cutaneous inflammation

• Published in: Biochemical and biophysical research communications Vol. 378; no. 4; pp. 777 - 782
• Main Authors: Abbondanzo, Susan J., Manfra, Denise J., Chen, Shu-Cheng, Pinzon-Ortiz, Maria, Sun, Yongliang, Phillips, Jonathan E., Laverty, Maureen, Vassileva, Galya, Hu, Weiwen, Yang, Shijun, Gustafson, Eric L., Fine, Jay S., Hedrick, Joseph A.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 23.01.2009
• Subjects: Animals; CFA; Cytokines - blood; Dermatitis - genetics; Dermatitis - immunology; Freund's Adjuvant - immunology; Freund's Adjuvant - pharmacology; Gene Deletion; Inflammation; Knockout; Mice; Mice, Knockout; Neuromedin U receptor 1; Receptors, Neurotransmitter - genetics; Receptors, Neurotransmitter - physiology; Inflammation; Mice; Neuromedin U receptor 1; Knockout; CFA
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2008.11.148

Neuromedin U (Nmu) is a neuropeptide expressed primarily in the gastrointestinal tract and central nervous system. Previous reports have identified two G protein-coupled receptors (designated Nmur1 and Nmur2) that bind Nmu. Recent reports suggest that Nmu mediates immune responses involving mast cells, and Nmur1 has been proposed to mediate these responses. In this study, we generated mice with an Nmur1 deletion and then profiled the responses of these mice in a cutaneous inflammation model utilizing complete Freund’s adjuvant (CFA). We report here that mice lacking Nmur1 had normal inflammation responses with moderate changes in serum cytokines compared to Nmur1 +/+ littermates. Although differences in IL-6 were observed in mice lacking Nmu peptide, these mice exhibited a normal response to CFA. Our data argues against a major role for Nmur1 in mediating the reported inflammatory functions of NmU.