Candida albicans populations present in the mammalian gastrointestinal tract are a major source of candidemia and subsequent severe invasive candidiasis in those individuals with acquired or congenital immune defects. Understanding the mechanisms used by this fungus to colonize this niche is, therefore, of primary importance to develop new therapeutic options that could lead to control its proliferation in the host. The recent popularization of models of commensalism in mice combined with the already powerful tools in C. albicans genetics allows to analyze the role of specific genes during colonization. Fitness can be analyzed for a specific C. albicans strain (test strain) by comparing its growth in vivo with an otherwise isogenic control strain via the analysis of the luminal content of the mouse gastrointestinal tract using flow cytometry, qPCR, or viable fungal cell counting. While all these procedures have limitations, they can be used to estimate the degree of adaptation of the test strain to the mammalian tract by determining its relative abundance with an internal control strain. By using specific genetically engineered C. albicans and mouse strains, antibiotic regimes, or even germ-free mice, this methodology allows to determine the role of the host immunological status, the bacterial microbiota, or individual fungal features (e.g., dimorphism) in the process of colonization of C. albicans of the mammalian gut.
Keywords: Adaptation; Candida albicans; Colonization; Commensalism; Competition assay; Fitness; Gastrointestinal tract.
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