Candida albicans is a common human gut commensal and opportunistic pathogen, capable of causing superficial to severe disseminated candidiasis in humans. In response to environmental cues either outside or within the gastrointestinal (GI) tract, the yeast becomes virulent and is able to damage murine intestinal epithelium through invasive filamentation. Previous research in the Kumamoto lab has identified the Dfi1 cell surface protein to be a key component of a signaling pathway that activates contact-dependent filamentation and has demonstrated an upregulation of lipid compounds in mice colonized with C. albicans. We propose that lipid compounds are being liberated from host epithelial cells through fungal-induced damage and hypothesize that the dfi1Δ C. albicans mutant should show reduced filamentation capability, thus lessening its ability to damage the murine intestinal tract through invasive filamentation and hydrolytic activity. The scope of this project is to characterize both WT and dfi1Δ mutant C. albicans damage capability on the intestinal epithelium using a human model of the intestinal epithelia derived from colonoids as well as a murine model.