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Calling a Truce: Enterococcus faecalis as a mediator between E. coli and C. albicans during polymicrobial CAUTIs

ABSTRACT: Polymicrobial catheter-associated urinary tract infections (CAUTIs) are a severe clinical burden. CAUTIs promotes colonization by different microbes, including E. faecalis, E. coli, and C. albicans. These mixed biofilms can compromise antimicrobial efficacy and promote resistance. Despite their prevalence, the cross-kingdom dynamics driving these infections within the catheterized bladder remain poorly understood. Using established in vitro and in vivo CAUTI models, we elucidate the complex, environment-dependent interactions governing these multispecies biofilms. We demonstrate that E. coli strongly antagonizes C. albicans, by limiting iron uptake, inhibiting filamentation, and inducing cell death. Crucially, we identify E. faecalis as a protective keystone species that mitigates this antagonism. E. faecalis facilitates multispecies coexistence by acting as a spatial bridge on the urothelium, enabling E. coli and C. albicans to co-localize rather than occupy segregated niches. These mechanistic insights into polymicrobial synergy and competition provide a crucial framework for developing targeted therapeutics against recalcitrant CAUTIs.

ORGANISM(S): Escherichia coli Enterococcus faecalis Candida albicans

PROVIDER: GSE329180 | GEO | 2026/04/27

REPOSITORIES: GEO

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Project description:The interaction of clinically relevant microorganisms is the focus of various studies, e.g. the interaction between the pathogenic yeast, Candida albicans, and the bacterium, Pseudomonas aeruginosa and these interactions can alter the outcome of infection, growth dynamics of each species and antimicrobial resistance of pathogens. During infection, both C. albicans and P. aeruginosa can elicit the release arachidonic acid (AA) from host cells membranes through the action of phospholipases. This polyunsaturated fatty acid can be transformed into immune-modulating compounds, termed eicosanoids, by both host-derived and microbial-derived enzymatic reactions. In its free form, AA can affect the growth of both C. albicans and P. aeruginosa, inhibiting the morphogenesis of C. albicans as well as reducing resistance towards antifungal agents. However, the mechanism of this is unknown. Previous studies on the effect of polyunsaturated fatty acids have indicated a possible alteration in plasma membrane organisation and permeability. Our group aimed to address how AA affects C. albicans in both single species biofilms, as well as in polymicrobial biofilms with P. aeruginosa. RNAseq was performed on single and polymicrobial biofilms in the presence and absence of a sub-inhibitory (100 µM) concentration of AA. Differential expression was determined between C. albicans single species biofilms in the presence and absence of AA. Secondly, the influence of co-incubation of C. albicans with P. aeruginosa in the absence of AA was evaluated to identify novel facets of interaction not previously identified, and to establish a baseline to determine the effect of AA on C. albicans in polymicrobial biofilms. Lastly, the effect of AA on C. albicans in polymicrobial biofilms was determined through comparison with polymicrobial biofilms in the absence of AA. This study provides a comprehensive analysis of the effect of AA and both co-incubation of C. albicans with P. aeruginosa focused on the transcriptome.

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Calling a Truce: Enterococcus faecalis as a mediator between E. coli and C. albicans during polymicrobial CAUTIs

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