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Candida albicans Microarray studies: CAP2 (Wild type) vs. cap2D (Homozygous null mutant)

ABSTRACT: Transcriptome profiling to identify Cap2/Hap43 regulons in the human fungal pathogen Candida albicans: Wild type vs. cap2D grown in iron-depleted medium

ORGANISM(S): Candida albicans

PROVIDER: GSE28429 | GEO | 2011/05/25

SECONDARY ACCESSION(S): PRJNA139151

REPOSITORIES: GEO

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Candida albicans Microarray studies: CAP2 (Wild type) vs. cap2D (Homozygous null mutant)

Project description:Transcriptome profiling to identify Cap2/Hap43 regulons in the human fungal pathogen Candida albicans: Wild type vs. cap2D grown in iron-depleted medium Two-condition experiment, WT vs. cap2D cells. Biological replicates: Wild-type and cap2D, independently grown in iron-depleted medium and harvested. One replicate per array. Hybridization was repeated (technical replicate) for each biological replicate.

2011-05-24 | E-GEOD-28429 | biostudies-arrayexpress

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Project description:Candida albicans Microarray studies: CAP2 (Wild type) vs. cap2D (Homozygous null mutant)

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Genome-wide transcriptional profiling of human PBMCs stimulated with Candida albicans and non-fungal inflammatory stimuli

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Augmented enterocyte damage during Candida albicans and Proteus mirabilis coinfection

Project description:The human gut acts as the main reservoir of microbes and a relevant source of life-threatening infections, especially in immunocompromised patients. There, the opportunistic fungal pathogen Candida albicans adapts to the host environment and additionally interacts with residing bacteria. We investigated fungal-bacterial interactions by coinfecting enterocytes with the yeast Candida albicans and the Gram-negative bacterium Proteus mirabilis resulting in enhanced host cell damage. This synergistic effect was conserved across different P. mirabilis isolates and occurred also with non-albicans Candida species and C. albicans mutants defective in filamentation or candidalysin production. Using bacterial deletion mutants, we identified the P. mirabilis hemolysin HpmA to be the key effector for host cell destruction. Spatially separated coinfections demonstrated that synergism between Candida and Proteus is induced by contact, but also by soluble factors. Specifically, we identified Candida-mediated glucose consumption and farnesol production as potential triggers for Proteus virulence. In summary, our study demonstrates that coinfection of enterocytes with C. albicans and P. mirabilis can result in increased host cell damage which is mediated by bacterial virulence factors as a result of fungal niche modification via nutrient consumption and production of soluble factors. This supports the notion that certain fungal-bacterial combinations have the potential to result in enhanced virulence in niches such as the gut and might therefore promote translocation and dissemination.

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