Abstract
Candida albicans is an opportunist pathogen responsible for a large spectrum of infections, from superficial mycosis to systemic diseases known as candidiasis. Its ability to grow in different morphological forms, such as yeasts or filamentous hyphae, contributes to its survival in diverse microenvironments. Iron uptake has been associated with virulence, and C. albicans has developed elaborate strategies for acquiring iron from its host. In this work, we analyze the metabolic changes in response to changes in iron content in the growth medium and compare C. albicans adaptation to the presence or absence of iron. Functional and morphological studies, correlated to a quantitative proteomic analysis, were performed to assess the specific pathways underlying the response to iron, both in the yeast and filamentous forms. Overall, the results show that the adaptive response to iron is associated with a metabolic remodeling affecting the energetic pathways of the pathogen. This includes changes in the thiol‐dependent redox status, the activity of key mitochondrial enzymes and the respiratory chain. Iron deficiency stimulates bioenergetic pathways, whereas iron‐rich condition is associated with greater biosynthetic needs, particularly in filamentous forms. Moreover, we found that C. albicans yeast cells have an extraordinary capability to adapt to changes in environmental conditions.
Highlights
Candida albicans, one of the predominant opportunist pathogen yeast, is a commensal organism that colonizes the mucosal surfaces of the oral and vaginal cavities and the digestive tract
Our results suggest that iron induces a metabolic remodeling response and that C. albicans yeast cells can adapt to a large set of iron conditions
It is crucial to understand the metabolic changes associated with the response of C. albicans to changes in iron content of the growth medium and to identify some of the biochemical targets involved in this response
Summary
One of the predominant opportunist pathogen yeast, is a commensal organism that colonizes the mucosal surfaces of the oral and vaginal cavities and the digestive tract. A striking feature of C. albicans is its ability to grow in various morphological forms, including unicellular budding yeasts, filamentous pseudohyphae and true hyphae, and some less common forms, such as chlamydospores and opaque cells (Berman, 2006; Calderone, 2002; Gow, 1997; Sudbery, Gow, & Berman, 2004; Whiteway & Oberholzer, 2004) This ability to switch between forms is a key survival mechanism in the hostile host environment. It has recently been shown that limiting iron levels with the novel chelator DIBI (a hydroxypyridinone-class chelator) inhibits C. albicans growth and increases susceptibility to azoles in a murine model of vaginitis (Savage et al, 2018) This may account for the greater susceptibility to C. albicans infection of patients suffering from diseases with symptoms of iron overload (Bullen, Rogers, Spalding, & Ward, 2006). Infection seems to disturb global iron homeostasis in the host in a murine model of candidiasis (Potrykus et al, 2013)
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