Distinct Roles of Candida albicans-Specific Genes in Host-Pathogen Interactions

Wilson, Duncan; Mayer, François; Miramón, Pedro; Citiulo, Francesco; Slesiona, Silvia; Jacobsen, Ilse D.; Hube, Bernhard

doi:10.1128/ec.00051-14

Cited by 12 publications

(11 citation statements)

References 53 publications

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“…The differential capacity of the major human pathogenic species to utilize differing iron sources as described above is in line with the concept of independently evolved virulence of human fungal pathogens (Bowman, Taylor and White 1992 ; Wilson et al. 2014 ) and it would appear that different human fungal pathogens utilize different strategies to secure iron from their hosts.…”

Section: Introductionsupporting

confidence: 61%

Essential metals at the host-pathogen interface: nutritional immunity and micronutrient assimilation by human fungal pathogens

Crawford

Wilson

2015

FEMS Yeast Research

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The ability of pathogenic microorganisms to assimilate sufficient nutrients for growth within their hosts is a fundamental requirement for pathogenicity. However, certain trace nutrients, including iron, zinc and manganese, are actively withheld from invading pathogens in a process called nutritional immunity. Therefore, successful pathogenic species must have evolved specialized mechanisms in order to adapt to the nutritionally restrictive environment of the host and cause disease. In this review, we discuss recent advances which have been made in our understanding of fungal iron and zinc acquisition strategies and nutritional immunity against fungal infections, and explore the mechanisms of micronutrient uptake by human pathogenic fungi.

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Section: Introductionsupporting

confidence: 61%

Essential metals at the host-pathogen interface: nutritional immunity and micronutrient assimilation by human fungal pathogens

Crawford

Wilson

2015

FEMS Yeast Research

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“…HUVECs have already been extensively used to characterize endothelial cell FGF-2 expression [41], and to investigate C. albicans-endothelial cell interactions [42][43][44][45]. As the results in Figure 1a and 1b show, C. albicans can induce FGF-2 secretion only in the hyphal form.…”

Section: Discussionmentioning

confidence: 96%

<em></em><em>Candida albicans </em>Morphology Dependent Host FGF-2 Response as a Potential Therapeutic Target

Vellanki¹,

Huh²,

Saville³

et al. 2019

Preprint

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Angiogenesis mediated by proteins such as Fibroblast Growth Factor – 2 (FGF-2) is a vital component of normal physiological processes and has also been implicated in contributing to disease state associated with various microbial infections. Previous studies by our group and others have shown that Candida albicans, a common agent of candidiasis, induces FGF-2 expression in vitro, and angiogenesis in brains and kidneys during systemic infections. However, the underlying mechanism(s) via which the fungus increases FGF-2 expression and the role(s) that FGF-2/angiogenesis plays in C. albicans disease remain unknown. Here we show, for the first time, that C. albicans hyphae (and not yeast cells) increase the FGF-2 response in human endothelial cells. Moreover, candidalysin, a toxin secreted exclusively by C. albicans in the hyphal state is required to induce this response. Our in vivo studies show that, in the systemic C. albicans infection model, mice treated with FGF-2 exhibit significantly higher mortality rates when compared to untreated mice not given the angiogenic growth factor. Even treatment with fluconazole could not fully rescue infected animals that were administered FGF-2. Our data suggest that the increase of FGF-2 production/angiogenesis induced by candidalysin contributes to the pathogenicity of C. albicans.

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“…Metabolic adaptation and the ability to respond to environmental stresses have been extensively associated with C. albicans pathogenesis [26,27]. The capacity of C. albicans to sense changes in the environment and straight away respond, adapting to the new conditions as well as the capability to use a wide variety of nutrients, allows this fungus to inhabit different niches and cause diverse diseases.…”

Section: Discussionmentioning

confidence: 99%

Deletion of the SKO1 Gene in a hog1 Mutant Reverts Virulence in Candida albicans

Urrialde

Prieto

Hidalgo-Vico

et al. 2019

JoF

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Candida albicans displays the ability to adapt to a wide variety of environmental conditions, triggering signaling pathways and transcriptional regulation. Sko1 is a transcription factor that was previously involved in early hypoxic response, cell wall remodeling, and stress response. In the present work, the role of sko1 mutant in in vivo and ex vivo studies was explored. The sko1 mutant behaved as its parental wild type strain regarding the ability to colonize murine intestinal tract, ex vivo adhesion to murine gut epithelium, or systemic virulence. These observations suggest that Sko1 is expendable during commensalism or pathogenesis. Nevertheless, the study of the hog1 sko1 double mutant showed unexpected phenotypes. Previous researches reported that the deletion of the HOG1 gene led to avirulent C. albicans mutant cell, which was, therefore, unable to establish as a commensal in a gastrointestinal murine model. Here, we show that the deletion of sko1 in a hog1 background reverted the virulence of the hog1 mutant in a systemic infection model in Galleria mellonella larvae and slightly improved the ability to colonize the murine gut in a commensalism animal model compared to the hog1 mutant. These results indicate that Sko1 acts as a repressor of virulence related genes, concluding that Sko1 plays a relevant role during commensalism and systemic infection.

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Distinct Roles of Candida albicans-Specific Genes in Host-Pathogen Interactions

Cited by 12 publications

References 53 publications

Essential metals at the host-pathogen interface: nutritional immunity and micronutrient assimilation by human fungal pathogens

Essential metals at the host-pathogen interface: nutritional immunity and micronutrient assimilation by human fungal pathogens

<em></em><em>Candida albicans </em>Morphology Dependent Host FGF-2 Response as a Potential Therapeutic Target

Deletion of the SKO1 Gene in a hog1 Mutant Reverts Virulence in Candida albicans

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