The Mouse/Histology Core B will provide SAMPI/YitFc (SAMP) mice and other mouse modesi of experimental CD for use in each of the individual projects. Maintaining the SAMP breeding colony and experimental animals in a common centralized facility under uniform environmental conditions is crucial to the success of the program. Centralization of mouse production will also reduce costs by eliminating redundant breeding colonies, and ulfimately reduce the numbers of mice required by ensuring efficient utilization by each of the projects.
A second aim i s to provide centralized histological services and assistance with immunohistochemistry, digital fluorescence and brightfield microscopy for each of the projects.
The third aim of the Core is to provide centralized histopathological analyses of inflammation and other morphological parameters to invesfigators within the program. A centralized core component for analysis of the histopathological features of ileitis and colitis in this model will provide a common framework for interpretation of data generated by each of the four projects. A strength of this component is the availability of an experienced Gl pathologists. Dr. Xin, to perform histopathological scoring of samples to each of the projects and to provide ongoing consultative service to the projects conceming the pathological features of disease in this model. The forth aim is to provide consultation and teaching on immunohistochemical techniques and marker-assisted breed strategies for the generation of mutant congenic mouse strains that will be useful to projects within the program. Transfer of these induced mutations into an appropriate background can be accomplished in 5 generations. Dr. Pizarro will direct the core. A committee consisting of the core director and project leaders, will address routine quality control and prioritization issues. An oversight committee will review the operation of the core on a yearly basis.
CD affects more than 500,000 individuals in the US and incurs significant costs to society. Understanding the precise mechanisms and immune defects that cause the disease will allow us to develop better therapies and begin to develop a cure for this devastating disease.
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|Tigno-Aranjuez, Justine T; Benderitter, Pascal; Rombouts, Frederik et al. (2014) In vivo inhibition of RIPK2 kinase alleviates inflammatory disease. J Biol Chem 289:29651-64|
|Corridoni, Daniele; Arseneau, Kristen O; Cominelli, Fabio (2014) Functional defects in NOD2 signaling in experimental and human Crohn disease. Gut Microbes 5:340-4|
|Corridoni, Daniele; Arseneau, Kristen O; Cominelli, Fabio (2014) Inflammatory bowel disease. Immunol Lett 161:231-5|
|Cavalcanti, Elisabetta; Vadrucci, Elisa; Delvecchio, Francesca Romana et al. (2014) Administration of reconstituted polyphenol oil bodies efficiently suppresses dendritic cell inflammatory pathways and acute intestinal inflammation. PLoS One 9:e88898|
|Goodman, Wendy A; Pizarro, Theresa T (2013) Regulatory cell populations in the intestinal mucosa. Curr Opin Gastroenterol 29:614-20|
|Pastorelli, Luca; De Salvo, Carlo; Vecchi, Maurizio et al. (2013) The role of IL-33 in gut mucosal inflammation. Mediators Inflamm 2013:608187|
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