Title of the presentation: Candida tropicalis-derived vitamin B3 exerts protective effects against intestinal inflammation
Speaker: Ha T. Doan
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Abstract of this talk: Mycobiota are an integral part of gut microbiota, and their dysbiosis leads to gastrointestinal disorders. Candida tropicalis is increasingly recognized as a major opportunistic pathogen that causes nosocomial bloodstream fungal infections in most tropical countries. However, how commensal C. tropicalis interacts with the intestinal barrier and mucosal immunity remains poorly understood during inflammation. In this study, we demonstrated that the reference strain of C. tropicalis (MYA-3404) ameliorated intestinal inflammation in murine models of chemically induced colitis and bacterial infection. Intestinal colonization of C. tropicalis robustly upregulated the expression of IL-17A and IL-22 by Th17 cells, γδ T cells, and ILC3 to increase barrier function and promote proliferation of intestinal epithelial cells in the colon. Metabolomics analysis of fecal samples from mice colonized with C. tropicalis revealed alterations in vitamin B3 metabolism, facilitating conversion of nicotinamide to nicotinic acid. Although nicotinamide worsened colitis, treatment with nicotinic acid alleviated disease symptoms and enhanced epithelial proliferation and Th17 cell differentiation. Blockade of nicotinic acid production with nicotinamidase inhibitors abrogated the protective effects against colitis induced with C. tropicalis. Notably, a clinical C. tropicalis strain isolated from patients with candidemia lacked the protective effects against murine colitis observed with the reference strain. In summary, our findings highlight a novel role for C. tropicalis in resolving intestinal inflammation by modulating vitamin B3 metabolism.
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