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Regulation of miRNAs in macrophages in response to Candida albacans

ABSTRACT: In this study we have analysed the regulation of miRNA in bone marrow derived macrophages in response to the fungal pathogen heat killed Candida albicans and bacterial cell wall component, LPS. The aim of the study was to identify and validate miRNAs involved in the innate immune system in response to fungal and bacterial stimuli and investigate potential mechanisms for their transcription.

ORGANISM(S): Mus musculus

PROVIDER: GSE21970 | GEO | 2010/12/31

SECONDARY ACCESSION(S): PRJNA126785

REPOSITORIES: GEO

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Regulation of miRNAs in macrophages in response to Candida albacans

Project description:In this study we have analysed the regulation of miRNA in bone marrow derived macrophages in response to the fungal pathogen heat killed Candida albicans and bacterial cell wall component, LPS. The aim of the study was to identify and validate miRNAs involved in the innate immune system in response to fungal and bacterial stimuli and investigate potential mechanisms for their transcription. Three mice were used as 3 biological replicates. The bone marow derived macrophages from each mouse were divided into two and either left untreated or were stimulatred for 16 h with heat killed Candida albicans.

2010-12-31 | E-GEOD-21970 | biostudies-arrayexpress

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

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

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