Our laboratory focuses on the role and regulation of sphingolipids and their metabolizing enzymes in the pathobiology of inflammation. Specifically, our interests are in gastrointestinal inflammation and inflammatory bowel disease. We employ both in vitro and in vivo model systems to examine the role of dietary modulation on sphingolipid metabolism and inflammation. In our pursuits, we utilize cell lines, intestinal organoids, in vivo models, and biobanked samples from patients with IBD and colorectal cancer to determine the effects of high fat diets and dietary fatty acids on sphingolipid metabolism and intestinal pathobiology. Moreover, we utilize unbiased “Omics” approaches in our research efforts, specifically lipidomics, proteomics and phospho-proteomics, in order to define novel mechanisms, interventions, therapeutic targets and biomarkers for intestinal pathobiologies.
EDUCATION & PROFESSIONAL TRAINING • Post-Doctoral Training, Sphingolipids and Animal Models of Disease, Medical University of South Carolina • Ph.D., Pharmacology and Toxicology, Washington State University • B.S., Marine Biology, University of North Carolina at Wilmington RESEARCH & INTERESTS The long-term research goals of the Snider lab are to define the roles of lipid metabolic pathways centered on bioactive sphingolipids in intestinal biology and pathobiology and determine the mechanisms involved. Sphingolipids, long thought to be only structural components of cell membranes, have emerged over the last two decades as bioactive lipids with distinct and important biological functions. Dietary fatty acids are incorporated into ceramide, the central lipid in sphingolipid metabolism, via de novo synthesis and via incorporation by enzymes called ceramide synthases (CerS). Ceramide in turn serves as a metabolic hub for the synthesis of several classes of sphingolipids. These bioactive lipids are involved in diverse cellular and biologic functions including insulin resistance, cardiovascular disease, inflammation and cancer. The Snider lab has demonstrated the importance of several sphingolipids and their metabolic enzymes as key regulators in inflammatory bowel disease, as well as colon cancer and colitis-associated colon cancer. The Snider lab has recently begun demonstrating that specific dietary fatty acids increase specific sphingolipids leading to in the intestinal epithelium in cells and in vivo. Current research in the Snider lab focus builds on this foundation. The three main projects in the lab examine: 1) Effects of dietary fatty acids on sphingolipid metabolism in ER stress and inflammation. 2) Roles of dietary fatty acids and sphingolipids in animal models of inflammation and colitis-associated cancer. 3) Roles for sphingolipids and their metabolizing enzymes in intestinal biology and pathobiology. In these pursuits, the Snider lab utilizes cell lines, intestinal organoids (murine and human), in vivo models, and biobanked samples from patients with inflammatory bowel disease and colorectal cancer to determine the effects of high fat diets and dietary fatty acids on sphingolipid metabolism and intestinal pathobiology. Moreover, the use of unbiased “Omics” approaches in their research efforts, specifically lipidomics, proteomics and phospho-proteomics, is beginning to enable the discovery of novel mechanisms, interventions, therapeutic targets and biomarkers for intestinal pathobiologies.