Journal
CELLULAR MICROBIOLOGY
Volume 17, Issue 4, Pages 445-450Publisher
WILEY
DOI: 10.1111/cmi.12388
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Funding
- Wellcome Trust [086558, 080088, 102705]
- Wellcome Trust Strategic Award [097377]
- University of Aberdeen
- National Institute of Allergy and Infectious Diseases [5R01AI083344]
- Voelcker Young Investigator Award from the Max and Minnie Tomerlin Voelcker Fund
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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.
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