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Updated: Jan 11, 2026
Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
Published on: March 19, 2019
Synergistic interactions between Candida albicans and Enterococcus faecalis promote toxin-dependent host cell damage
Mario Kapitan1,2,3, Maria Joanna Niemiec1,2, Nicolas Millet4,5
1Research Group Microbial Immunology, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute, Jena 07745, Germany.
Abstract:
The fungus Candida albicans and the Gram-positive bacterium Enterococcus faecalis share mucosal niches in the human body. As opportunistic pathogens, both are found to expand population size during dysbiosis, and can cause severe systemic infections in susceptible individuals. Here, we show that the presence of C. albicans results in increased host cell damage by E. faecalis. Furthermore, E. faecalis aggravates oropharyngeal candidiasis in mice. Increased damage is mediated by enterococcal cytolysin, and involves both physical interaction and altered glucose availability. Physical interaction promotes accumulation of bacteria on host cells, facilitating contact of cytolysin with host cells. Glucose depletion by the metabolic activity of the fungus sensitized host cells to cytolysin. This work illustrates how a complex interplay between fungi and bacteria can result in detrimental consequences for the host.
Insights
Candida albicans and Enterococcus faecalis coinfection increases host cell damage. The fungus alters glucose availability and promotes bacterial adherence, enhancing pathogen-induced damage and oropharyngeal candidiasis severity.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Candida albicans and Enterococcus faecalis are opportunistic pathogens sharing mucosal sites.
- Both microbes can cause severe infections, particularly during dysbiosis.
Purpose of the Study:
- To investigate the synergistic interactions between C. albicans and E. faecalis.
- To elucidate the mechanisms by which C. albicans exacerbates E. faecalis-mediated host cell damage.
Main Methods:
- In vitro co-culture models to assess host cell damage.
- Murine model of oropharyngeal candidiasis to evaluate disease severity.
- Analysis of bacterial adherence and glucose availability.
Main Results:
- C. albicans presence significantly increased host cell damage caused by E. faecalis.
- E. faecalis aggravated oropharyngeal candidiasis in a mouse model.
- Enterococcal cytolysin mediated increased damage, enhanced by physical interaction and glucose depletion.
Conclusions:
- Fungal-bacterial coinfections can lead to amplified pathogenesis.
- Interactions involving physical contact and nutrient availability are critical in polymicrobial infections.
- Understanding these complex interplays is crucial for developing effective therapeutic strategies.
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