To survive, fungal pathogens acquire nutrients from their environment to support basic biological processes. These nutrients include transition metals like copper (Cu) and iron (Fe), but due to their redox activity, these metals can become toxic if misappropriated. The host immune system exploits this delicate balance by manipulating metal availability at the host-pathogen interface. In turn, pathogens have developed mechanisms for tolerating metal starvation or excess and are well-equipped to survive these harsh territories. We posited that when faced with antifungal drug stress, a pathogen’s access to essential metals could make or break its ability to survive. In this work, we describe how metal availability impacts the response of fungal pathogen <i>Candida albicans </i>to treatment with the antifungal drug fluconazole, a mainstay in antifungal therapy. Overall, we establish that fluconazole both affects and is affected by cellular Cu machinery, and that the availability of Cu in the growth environment further modulates these effects, resulting in metal-mediated outcomes of drug treatment.

Metals as mediators in the cross-talk betwen drug and fungal pathogen

2019 Spring National Meeting

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