The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonization and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild-type and morphological mutants of C.albicans in an established model of GI tract colonization, induced following antibiotic treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C.albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C.albicans, and have implications for our understanding of human disease. Candida albicans is a commensal of the human gastrointestinal (GI) tract but can also spread from this site to cause systemic disease following immune perturbation. Here, using morphologically-locked strains we show that although the yeast form is favoured in the GI tract, both the yeast and hyphal forms can disseminate from this site to distal tissues in healthy animals. Finally, we show that Th17 immunity has no role in fungal colonisation or dissemination from the GI tract.
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