The overall research interest of the applicant is on the cellular and molecular pathogenesis of infections with enteric pathogens and the mechanisms governing intestinal inflammatory responses. The long-germ objective is to build an externally funded independent research program in mucosal immunology and mouse pathobiology research at a major U.S. academic institution. The use of mouse models of intestinal infection and inflammation is an integral component of this research program. Studies in physiologically complex model systems are necessary to validate or discard hypothesis generated in cell culture studies, and to develop new strategies for treatment and prevention of infections with foodborne pathogens and attenuation of intestinal inflammation in patients with idiopathic inflammatory bowel disease (IBD). The proposal has two major objectives: 1. To teach courses in mouse pathobiology research and mentor new investigators, both pre and postdoctoral, at UCSD in conducting specific projects in mouse pathobiology research. 2. Conduct studies to define the physiological functions of the thromboxane A2 receptor, TP, in regulating intestinal inflammation in murine models. Preliminary results show that TP is an important proinflammatory regulator in experimental colitis models, suggesting that it might be a promising target for anti-inflammatory treatment strategies in IBD. The applicant is Director of a Mouse Model Core within a NIH-funded P01 Program Project Grant in Mucosal Immunology at UCSD, and has established the necessary laboratory infrastructures for conducting mouse pathobiology research and mentoring of new investigators. The award will provide salary and technical support for the applicant to devote a greater amount of time than otherwise possible to the development of the mouse pathobiology research program of the Mouse Model Core and the mentoring of new investigators in conducting high-quality mouse pathobiology research.
NIH ExPorter
NIH ExPorter