Bio

Dr. Ying Zhu is a postdoctoral scholar in the Rosen Lab, Department of Pediatrics, Division of Gastroenterology, Hepatology & Nutrition at Stanford University. She earned her PhD in 2023 from the Friedman School of Nutrition Science and Policy at Tufts University. In the Rosen Lab, Dr. Zhu investigates intestinal epithelial metabolic dysfunction in pediatric inflammatory bowel diseases and chronic intestinal inflammation. Her primary objective is to characterize metabolic reprogramming in ulcerative colitis epithelium and to identify defects that persist in patient-derived organoids, or colonoids. Her broader research interests lie in the interplay between intestinal energy metabolism and epithelial barrier homeostasis in children with ulcerative colitis.

Institute Affiliations

Boards, Advisory Committees, Professional Organizations

  • Member, American Gastroenterological Association (2024 - Present)
  • Member, American Society of Nutrition (2017 - Present)

Stanford Advisors

All Publications

  • Follicle-associated epithelial tuft cells amplify type 2 mucosal immunity and IgA production. Science immunology Barrón, G. M., Jayewickreme, R. D., Tran, H. H., Thompson, T. W., Narasimhan, R., Zhu, Y., DeSchepper, L. B., Habashi, D., Nico, K. F., Tyner, M. D., Tierney, F. M., Billipp, T. E., Rosen, M. J., Monack, D. M., von Moltke, J., Howitt, M. R. 2026; 11 (124): eaee1358

    Abstract

    Peyer's patches (PPs) in the intestinal mucosa coordinate antibody responses to luminal microbes and dietary antigens. The follicle-associated epithelium (FAE) is traditionally recognized by the presence of microfold cells (M cells) that mediate antigen sampling in PPs. By analyzing Gfi1b-eGFP reporter mice and human PP biopsies, we identified tuft cells as an additional, evolutionarily conserved FAE population that regulates mucosal immunity. Using mouse models and intestinal organoids, we demonstrate that M cells and tuft cells are distinct lineages arising from Pou2f3+ progenitors, whose differentiation is reciprocally regulated by RANKL and interleukin-13 (IL-13), respectively. Tuft cell-derived IL-25 activates type 2 innate lymphoid cells (ILC2s) in PPs. Furthermore, IL-13 production by ILC2 enhances immunoglobulin A class switching and antigen-specific immunity. These findings reveal a dual surveillance system in the FAE, where developmentally related epithelial lineages use distinct mechanisms to coordinate mucosal immunity.

    View details for DOI 10.1126/sciimmunol.aee1358

    View details for PubMedID 42853963

  • Patient-derived colon epithelial organoids reveal lipid-related metabolic dysfunction in pediatric ulcerative colitis. Nature communications Ojo, B. A., Zhu, Y., Heo, L., Fox, S. R., Qiao, Y., Waddell, A., Moreno-Fernandez, M. E., Gibson, M., Tran, T., Dunn, A. L., Elknawy, E. I., Saini, N., López-Rivera, J. A., Divanovic, S., Dai, Y., de Jesus Perez, V. A., Rosen, M. J. 2025; 16 (1): 11026

    Abstract

    Ulcerative colitis (UC) is associated with epithelial metabolic derangements which exacerbate gut inflammation. Here, we develop colon organoid (colonoid) lines from pediatric patients with endoscopically active UC, inactive UC, and those without intestinal inflammation to interrogate functional metabolic differences in the colon epithelia. We demonstrate that active UC colonoids exhibit hypermetabolic features and cellular stress, specifically during differentiation. Hypermetabolism in active UC colonoids is driven, in part, by increased proton leak, and excess lipid accumulation. Active UC colonoids exhibit heightened activation of the master lipid regulator PPAR-α and its transcriptional pathways. Pharmacological PPAR-α inhibition limits lipid accumulation, induces a metabolic shift towards glucose utilization, suppresses hypermetabolism, and reduces chemokine secretion and cellular stress markers. Collectively, our findings identify lipid-related metabolic dysfunction as a key pathologic feature of the pediatric UC epithelium and highlight the potential of patient-derived colonoids as a preclinical model for evaluating epithelial-targeted therapies addressing this dysfunction.

    View details for DOI 10.1038/s41467-025-65988-2

    View details for PubMedID 41372139

    View details for PubMedCentralID PMC12695892