Abstract
The human fungal pathogen Candida albicans (C. albicans) causes invasive candidiasis, characterized by fatal organ failure due to disseminated fungal growth and inflammatory damage. To better understand fungal pathogenicity mechanisms and host protective responses, a murine model of invasive candidiasis has been developed in which C. albicans is administered systemically via intravenous injection. In this infection model, all major tissues are seeded within 0-4h. Of all the peripheral organs, the kidneys provide the most favorable niches for fungal proliferation and the morphogenetic switch to a hyphal state. As a consequence, the kidneys are a focal point for analyzing many of the genetic and immunological factors that underlie disease progression. Herein, we describe a number of well-established techniques that allow investigation into specific mechanisms that impact host-pathogen interactions.
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