In high-income countries, the leading causes of death are non-communicable diseases, such as Inflammatory Bowel Disease (IBD), cancer, and cardiovascular disease. An important feature of most non-communicable diseases is inflammation-induced gut dysbiosis characterized by a shift in the microbial community structure from obligate to facultative anaerobes such as Proteobacteria. This microbial imbalance can contribute to disease pathogenesis due to either a microbiota-derived metabolite being depleted or produced at a harmful concentration. However, little is known about the mechanism by which inflammation mediates changes in the host physiology to induce disruption of the microbial ecosystem in our large intestine leading to disease.
Our group uses a multidisciplinary approach combining microbiology, molecular biology, cell biology, immunology, and pathology to understand how inflammation-dependent changes in host metabolism can result in gut dysbiosis and increased risk of non-communicable disease. Specifically, we used various mouse models, including diet-induced-obesity, chemical-induced colitis, and germ-free animals, to identify metabolic pathways in the gut bacteria and in the host response to microbiota-derived metabolites that will aid in the prevention of human disease. Our group also tries to figure out the mechanisms by which gut microbes adapt and overcome this harsh intestinal inflammatory condition by regulating their metabolism and gene expression.
Another arm of our research program focuses on how intestinal inflammation caused by the bacterial pathogen Salmonella enterica serovar Typhimurium induces changes in host physiology and how these changes can cause disruption of the microbial ecosystem (microbiota) in our large intestine and promote pathogen colonization and disease.

• ㆍHost-Microbe Interaction
• ㆍBacterial Physiology and Metabolism
• ㆍBacterial Pathogenesis
• ㆍMolecular Genetics of Bacteria
• ㆍRole of gut microbiota in high-fat diet-induced obesity and non-communicable diseases

• ㆍShelton CD and Yoo W et al. (2023) An early-life microbiota-metabolite protects against obesity by regulating intestinal lipid metabolism. Cell Host & Microbe 31(10):1604-1619.e10.
• ㆍShelton CD and Yoo W et al. (2022) Salmonella enterica serovar Typhimurium uses anaerobic respiration to overcome propionate-mediated colonization resistance. Cell Reports 38(1): 110180
• ㆍYoo W et al. (2021) High-fat diet-induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide. Science 373(6556): 813-818

• ㆍB.S., Chung-Ang University, Korea (2011)
• ㆍPh.D., Seoul National University, Korea (2017)

• ㆍ2017.3-2017.8 : Postdoctoral Researcher (Seoul National University, Korea)
• ㆍ2017.9-2018.8 : Postdoctoral Researcher (University of California at Davis, USA)
• ㆍ2018.9-2022.8 : Postdoctoral Researcher (Vanderbilt University Medical Center, USA)
• ㆍ2022.9-2023.2 : Research Instructor (Vanderbilt University Medical Center, USA)
• ㆍ2023.2-Present : Assistant Professor (POSTECH, Korea)
• ㆍ2023.9-Present : Adjunct Professor (Yonsei University, Korea)

• ㆍPostdoctoral Fellowship Program (Nurturing Next-generation Researchers) in 2020 granted by National Research Foundation of Korea (NRF) (2020)
• ㆍSidney P. Colowick Outstanding Postdoc Award in the Division of Molecular Pathogenesis, Vanderbilt University Medical Center, USA (2021)
• ㆍSingsong Award for Young Scientist, The Korean Society for Microbiology and Biotechnology (2022)

• ㆍHow do the host and the gut microbiota work together to promote health?
• ㆍWhat are the mechanisms leading to gut dysbiosis during inflammation?
• ㆍCan we identify the metabolic pathways in gut bacteria and the host response to microbiota-produced metabolites that will aid in the prevention of human diseases?
• ㆍCan we prevent gut dysbiosis and non-communicable diseases by targeting host epithelial metabolism?
• ㆍWhich mechanisms are used by enteric pathogens (e.g., Salmonella Typhimurium) to overcome microbiota-mediated colonization resistance?