Education & Certifications

  • B.S., Duke University, Biology (2019)

Contact

  • Academic
    youlimk@stanford.edu
    University - Student Department: Microbiology and Immunology Position: Graduate

Additional Info

  • Mail Code: 5124

All Publications

  • Accessible homeostatic gastric organoids reveal secondary cell type-specific host-pathogen interactions in Helicobacter pylori infections. Nature communications Hofer, M., Kim, Y., Broguiere, N., Gorostidi, F., Klein, J. A., Amieva, M. R., Lutolf, M. P. 2025; 16 (1): 2767

    Abstract

    Despite the high prevalence of gastric diseases like gastric cancer and peptic ulcer disease attributed to Helicobacter pylori infections, there is still only a limited understanding of the underlying mechanisms. Existing in vitro models are either two-dimensional systems lacking the structural complexity of the gastric architecture, or complex three-dimensional systems that pose challenges for experimental access. In this study, we introduce a patterned homeostatic human gastric organoid-on-a-chip system with bilateral access that is capable of modeling H. pylori niche establishment and persistent colonization of the gastric epithelium. We show that in physiological apical acidic conditions, our organ-on-a-chip can generate pit cells of higher maturity in contrast to traditionally grown organoids. Upon infection with H. pylori for up to 6 days, these mature pit cells exhibit a distinctive response from other cell types, which was previously uncharacterized. Beyond its application in studying H. pylori infection, the increased structural and functional relevance of our model offers broader significance as a versatile platform for advancing our understanding of gastric epithelial cell interactions, gastric mucosal immunity, and host-pathogen interactions.

    View details for DOI 10.1038/s41467-025-57131-y

    View details for PubMedID 40113752

    View details for PubMedCentralID 502139

  • MYADM binds human parechovirus 1 and is essential for viral entry. Nature communications Qiao, W., Richards, C. M., Kim, Y., Zengel, J. R., Ding, S., Greenberg, H. B., Carette, J. E. 2024; 15 (1): 3469

    Abstract

    Human parechoviruses (PeV-A) are increasingly being recognized as a cause of infection in neonates and young infants, leading to a spectrum of clinical manifestations ranging from mild gastrointestinal and respiratory illnesses to severe sepsis and meningitis. However, the host factors required for parechovirus entry and infection remain poorly characterized. Here, using genome-wide CRISPR/Cas9 loss-of-function screens, we identify myeloid-associated differentiation marker (MYADM) as a host factor essential for the entry of several human parechovirus genotypes including PeV-A1, PeV-A2 and PeV-A3. Genetic knockout of MYADM confers resistance to PeV-A infection in cell lines and in human gastrointestinal epithelial organoids. Using immunoprecipitation, we show that MYADM binds to PeV-A1 particles via its fourth extracellular loop, and we identify critical amino acid residues within the loop that mediate binding and infection. The demonstrated interaction between MYADM and PeV-A1, and its importance specifically for viral entry, suggest that MYADM is a virus receptor. Knockout of MYADM does not reduce PeV-A1 attachment to cells pointing to a role at the post-attachment stage. Our study suggests that MYADM is a multi-genotype receptor for human parechoviruses with potential as an antiviral target to combat disease associated with emerging parechoviruses.

    View details for DOI 10.1038/s41467-024-47825-0

    View details for PubMedID 38658526

    View details for PubMedCentralID 6893760