My research focuses on elucidating how host–microbiota interactions regulate immune responses in chronic inflammatory diseases and cancer, with a particular emphasis on sphingolipid signaling and mucosal immunology. Our laboratory investigates the molecular mechanisms by which microbial communities and microbial metabolites influence intestinal and systemic immunity to drive disease progression.

In inflammatory bowel disease and colorectal cancer, we study how microbial pathogens and commensal bacteria reshape the intestinal immune microenvironment. Our work has demonstrated that enterotoxigenic Bacteroides fragilis induces epithelial sphingosine-1-phosphate (S1P) signaling to promote NKT cell- and Th17-mediated colorectal tumorigenesis, establishing a mechanistic link between microbial dysbiosis, lipid signaling, and cancer development.

A second major focus is tumor immunology, where we investigate how sphingolipid metabolism regulates the tumor immune microenvironment. We recently identified ceramide-mediated reprogramming of macrophages into immunosuppressive TREM2⁺ tumor-associated macrophages that promote CD8⁺ T-cell exhaustion, revealing new mechanisms of immune evasion and therapeutic resistance.

Our laboratory also studies the gut–liver axis in alcohol-associated liver disease (ALD) and metabolic dysfunction-associated steatohepatitis (MASH). We have identified key roles for microbial fucosylation, intestinal IgA responses, neutral ceramidase, and sphingolipid signaling in regulating gut barrier function, microbial homeostasis, and hepatic inflammation. Our current work integrates microbiome engineering, microbial glycans, and host lipid signaling to develop microbiome-based therapeutic strategies for chronic liver disease and cancer.