The primary goal of Core B is to provide individual projects with intestinal tissue, isolated cell populations, and functional genomic information from clinically characterized IBD patients and healthy controls. This core will overcome a widely acknowledged roadblock in the use of animal models - direcfing animal research to address questions that will be directly translatable to human IBD. The data and tissue banks and novel technologies developed through this core will allow investigators the opportunity to correlate molecular findings across model species to human diseases. Core B will leverage substanfial existing resources and expertise at UNC. There is an established infrastructure for obtaining and processing surgical resecfions and intestinal biopsies. The """"""""Tissue"""""""" component of Core B will process and provide frozen intestinal tissue;RNA and protein extracts from intestinal tissue, deidentified clinical information on disease phenotype, and at the request of invesfigators, isolated intestinal cell populations. Where required, the core will be able to provide matched serum in peripheral blood mononuclear cell populafions as well as DNA to correlate immunophenotype, clinical phenotype with genetic background. Understanding the molecular basis of human IBD is far from being achieved. High throughput assays that permit the identification of gene regulatory networks in a heterogeneous disease like IBD is of paramount importance to elucidate the pathogenic mechanisms of IBD and for the development of diagnostic tools and of innovative therapeutics. The """"""""Genomics"""""""" component of Core B will use complementary high throughput assays of chromatin status (FAIRE, and ChIP) and gene expression (RNA) from isolated single cells (murine and human), and clinically phenotyped pafients combined with deep sequencing. Each Project profits by centralized data processing and analysis that increases feasibility and efficiency, decreases costs for each Program Project investigator and limits variations that may occur from technical error. Furthermore, Core B capitalizes and builds on the financial commitments and technical expertise already made by the NIH (ENCODE, 1000 genomes, and HapMap projects) and the Carolina Center for Genome Sciences. Data generated by Core B will allow each investigator to study active regulatory elements in the genome at a level of detail yet to be performed.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Research Program Projects (P01)
Project #
Application #
Study Section
Special Emphasis Panel (ZDK1-GRB-6)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of North Carolina Chapel Hill
Chapel Hill
United States
Zip Code
Simon, Jeremy M; Davis, James P; Lee, Saangyoung E et al. (2016) Alterations to chromatin in intestinal macrophages link IL-10 deficiency to inappropriate inflammatory responses. Eur J Immunol 46:1912-25
Abdalla, Maisa; Sheikh, Shehzad Z (2016) Harnessing the Power of Posttranscriptional Gene Silencing in Crohn's Disease. Clin Transl Gastroenterol 7:e160
Koblansky, A Alicia; Truax, Agnieszka D; Liu, Rongrong et al. (2016) The Innate Immune Receptor NLRX1 Functions as a Tumor Suppressor by Reducing Colon Tumorigenesis and Key Tumor-Promoting Signals. Cell Rep 14:2562-75
Wu, Cong; Sartor, R Balfour; Huang, Kehe et al. (2016) Transient activation of mucosal effector immune responses by resident intestinal bacteria in normal hosts is regulated by interleukin-10 signalling. Immunology 148:304-14
Weiser, Matthew; Sheikh, Shehzad; Kochar, Bharati et al. (2016) O-004 Analysis of Chromatin and Transcriptional Profiles in Crohn's Disease Reveals Molecular Subclasses and Highlights Functional Regulatory Regions Implicated in Disease. Inflamm Bowel Dis 22 Suppl 1:S1-2
Marjoram, Lindsay; Alvers, Ashley; Deerhake, M Elizabeth et al. (2015) Epigenetic control of intestinal barrier function and inflammation in zebrafish. Proc Natl Acad Sci U S A 112:2770-5
Liu, Rongrong; Truax, Agnieszka D; Chen, Liang et al. (2015) Expression profile of innate immune receptors, NLRs and AIM2, in human colorectal cancer: correlation with cancer stages and inflammasome components. Oncotarget 6:33456-69
Wang, Liuyang; Oehlers, Stefan H; Espenschied, Scott T et al. (2015) CPAG: software for leveraging pleiotropy in GWAS to reveal similarity between human traits links plasma fatty acids and intestinal inflammation. Genome Biol 16:190
Jha, Sushmita; Pan-Yun Ting, Jenny (2015) Holding the inflammatory system in check: NLRs keep it cool. F1000Prime Rep 7:15
Mishima, Yoshiyuki; Liu, Bo; Hansen, Jonathan J et al. (2015) Resident bacteria-stimulated IL-10-secreting B cells ameliorate T cell-mediated colitis by inducing Tr-1 cells that require IL-27-signaling. Cell Mol Gastroenterol Hepatol 1:295-310

Showing the most recent 10 out of 19 publications