Abstract
Candida albicans is a member of the human microbiota, colonizing both the vaginal and gastrointestinal tracts. This yeast is devoid of a life style outside the human body and the mechanisms underlying the adaptation to the commensal status remain to be determined. Using a model of mouse gastrointestinal colonization, we show here that C. albicans stably colonizes the mouse gut in about 3 days starting from a dose as low as 100 cells, reaching steady levels of around 107 cells/g of stools. Using fluorescently labeled strains, we have assessed the competition between isogenic populations from different sources in cohoused animals. We show that long term (15 days) colonizing cells have increased fitness in the gut niche over those grown in vitro or residing in the gut for 1–3 days. Therefore, two distinct states, proliferation and adaptation, seem to exist in the adaptation of this fungus to the mouse gut, a result with potential significance in the prophylaxis and treatment of Candida infections.
Highlights
Fungal agents are an important cause of nosocomial infections, which are a primary health problem in several countries (Pfaller and Diekema, 2007; Alangaden, 2011)
Initial studies involved neonatal mice, the most common system uses adult mice with a significant chemotherapy-driven microbiota reduction (Kinneberg et al, 1999; Mellado et al, 2000; Wiesner et al, 2001). These models have enabled the definition of the role that neutrophils have in the control of C. albicans dissemination (Koh et al, 2008) as well as provided experimental support for the role that certain yeast may have in the control and outcome of C. albicans colonization (Jawhara and Poulain, 2007)
In this work we have addressed the temporal dependence of C. albicans adaptation to the mouse gastrointestinal tract
Summary
Fungal agents are an important cause of nosocomial infections, which are a primary health problem in several countries (Pfaller and Diekema, 2007; Alangaden, 2011). Initial studies involved neonatal mice (de Repentigny et al, 1992), the most common system uses adult mice with a significant chemotherapy-driven microbiota reduction (Kinneberg et al, 1999; Mellado et al, 2000; Wiesner et al, 2001) These models have enabled the definition of the role that neutrophils have in the control of C. albicans dissemination (Koh et al, 2008) as well as provided experimental support for the role that certain yeast may have in the control and outcome of C. albicans colonization (Jawhara and Poulain, 2007). Using this system and measuring competitive fitness between different fungal populations, we were able to show how C. albicans cells adapt to the commensal status in a timely fashion
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