Iron restriction to clinical isolates of Candida albicans by the novel chelator DIBI inhibits growth and increases sensitivity to azoles in vitro and in vivo in a murine model of experimental vaginitis.
Savage KA1, Parquet MDC1, Allan DS1, Davidson RJ2,3, Holbein BE1, Lilly EA4, Fidel PL Jr5.
Antimicrob Agents Chemother. 2018 May 29. pii: AAC.02576-17.
doi: 10.1128/AAC.02576-17.

Abstract
Candida albicans is an important opportunistic pathogen causing various human infections that are often treated with azole antifungals. The US CDC now regards developing candidal antifungal resistance as a threat, creating a need for new and more
effective antifungal treatments. Iron is an essential nutrient for all living cells and there is growing evidence that interference with iron homeostasis of C. albicans can improve its response to antifungals. This study was aimed at establishing whether
withholding iron by currently used medical iron chelators and the novel chelator DIBI could restrict growth and also enhance the activity of azoles against clinical isolates of C. albicans DIBI but not deferoxamine or deferiprone, inhibited growth of C.
albicans at relatively low concentrations in vitro and this inhibition was reversed by iron addition. DIBI in combination with various azoles demonstrated stronger growth inhibition than the azoles alone and greatly prolonged inhibition of cell
multiplication. In addition, administration of DIBI along with fluconazole (FLC) to mice inoculated with a FLC-sensitive isolate in a model of experimental C. albicans vaginitis showed markedly improved clearance of infection. These results suggest that
iron chelation by DIBI has the potential to enhance azole efficacy for the treatment of candidiasis.

PMID: 29844048 DOI: 10.1128/AAC.02576-17

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