The recent proliferation of increasingly sophisticated murine models of chronic, relapsing intestinal inflammation and new techniques to target genetic deletions and insertions to discrete cell types have dramatically improved our ability to more precisely evaluate mechanisms of immune-mediated intestinal inflammation and mucosal homeostasis. In parallel, non-mammalian animal models such as zebrafish have facilitated high-resolution in vivo imaging and expeditious, cost-effective manipulation of target genes, leading to rapid discovery of new gene functions and entirely novel pathways regulating homeostasis and response to injury. These increasingly relevant and sophisticated animal models have allowed investigators to very rapidly and precisely address pathogenic and protective pathways, to perform preclinical studies that lay the foundation for highly effective human translational research and dramatically accelerate the search for novel therapeutic agents for inflammatory bowel diseases (IBD) and other inflammatory disorders. However, to create compound mutant and reporter strains, the degree of complexity and the need for very complicated breeding strategies with resultant increased per diem costs have placed many of these potentially useful models out of range for investigators with traditional ROl grant support, whose budgets typically have limited supply and per diem resources. The Animal Models Core centralizes breeding, development, and maintenance of these extraordinarily useful but complex animal models into a single unit that increases efficiency, decreases costs for Program Project investigators and prevents phenotype variation between investigators by providing a single environment for each centrally housed line. The Animal Models Core leverages exceptional specific pathogen free and gnotobiotic animal facilities and expert personnel to provide high-quality essential resources and services to all four Projects.
|Camp, J Gray; Frank, Christopher L; Lickwar, Colin R et al. (2014) Microbiota modulate transcription in the intestinal epithelium without remodeling the accessible chromatin landscape. Genome Res 24:1504-16|
|Kanther, Michelle; Tomkovich, Sarah; Xiaolun, Sun et al. (2014) Commensal microbiota stimulate systemic neutrophil migration through induction of serum amyloid A. Cell Microbiol 16:1053-67|
|Steinbach, Erin C; Kobayashi, Taku; Russo, Steven M et al. (2014) Innate PI3K p110? regulates Th1/Th17 development and microbiota-dependent colitis. J Immunol 192:3958-68|
|Robbins, Gregory R; Wen, Haitao; Ting, Jenny P-Y (2014) Inflammasomes and metabolic disorders: old genes in modern diseases. Mol Cell 54:297-308|
|Zhang, Lu; Mo, Jinyao; Swanson, Karen V et al. (2014) NLRC3, a member of the NLR family of proteins, is a negative regulator of innate immune signaling induced by the DNA sensor STING. Immunity 40:329-41|