Investigating Neuro-Immune Regulation by Gut Fungi - PROJECT ABSTRACT Millions of Americans suffer from inflammatory bowel disease (IBD), a condition marked by intestinal inflammation and abdominal pain. While the impact of the gut microbiota in IBD has been widely studied, the gut fungal “mycobiata” —and particularly the species of fungus Candida albicans— has emerged as a potential critical factor in this disease. While recent studies have revealed elevated levels of Candida albicans in IBD patients correlate with increased inflammation, the mechanisms underlying this connection remain unclear. Our research investigates how Candida albicans colonization contributes to intestinal inflammation and abdominal pain in a murine model of fungal dysbiosis. Preliminary data suggest that fungal colonization induces neutrophil infiltration , driving inflammation and tissue damage. We hypothesize that this inflammatory environment affects several disease aspects, directly via the fungal toxin candidalysin, or indirectly, through key proinflammatory cytokines . To address these hypotheses, I will use cell culture and murine models to examine how fungal colonization and candidalysin production drive inflammation, receptor activation, or influence abdominal pain. By exploring the direct and indirect effects of fungal virulence factors on neuroimmunity, this work will advance the understanding of fungal-immune-neuronal interactions in IBD and will hopefully advance the search for new potential therapeutic targets .
