Abstract
Candida albicans as an opportunistic pathogen exploits the host immune system and causes a variety of life-threatening infections. The polymorphic nature of this fungus gives it tremendous advantage to breach mucosal barriers and cause oral and disseminated infections. Similar to C. albicans, Enterococcus faecalis is a major opportunistic pathogen, which is of critical concern in immunocompromised patients. There is increasing evidence that E. faecalis co-exists with C. albicans in the human body in disease samples. While the interactive profiles between these two organisms have been studied on abiotic substrates and mouse models, studies on their interactions on human oral mucosal surfaces are non-existent. Here, for the first time, we comprehensively characterized the interactive profiles between laboratory and clinical isolates of C. albicans (SC5314 and BF1) and E. faecalis (OG1RF and P52S) on an organotypic oral mucosal model. Our results demonstrated that the dual species biofilms resulted in profound surface erosion and significantly increased microbial invasion into mucosal compartments, compared to either species alone. Notably, several genes of C. albicans involved in tissue adhesion, hyphal formation, fungal invasion, and biofilm formation were significantly upregulated in the presence of E. faecalis. By contrast, E. faecalis genes involved in quorum sensing, biofilm formation, virulence, and mammalian cell invasion were downregulated. This study highlights the synergistic cross-kingdom interactions between E. faecalis and C. albicans in mucosal tissue invasion.
Highlights
Candida albicans resides as a commensal organism in the human microbiota and exists in homeostasis with the microbial flora and epithelial tissues in healthy individuals [1]
C. albicans interacts with the epithelia-associated proteins such as E-cadherin, which induces endocytosis and provides a mechanism for epithelial cell penetration [24]
Histological imaging of the infected tissues demonstrated that the surface erosion of tissues in the dual species biofilms of the reference strains (E. faecalis OG1RF and C. albicans SC5314) was similar to that observed with C. albicans alone, but greater than with E. faecalis alone (Figure 1)
Summary
Candida albicans resides as a commensal organism in the human microbiota and exists in homeostasis with the microbial flora and epithelial tissues in healthy individuals [1]. Overgrowth of specific bacterial species that establish mutualistic interactions with candida species results in increased tissue damage and invasion Such mutualism has been demonstrated extensively between C. albicans and commensal oral Streptococci in both in vitro and mouse models. Enterococcus faecalis, a Gram-positive bacterium, is known to cause several infections including endocarditis, bacteremia, abdominal abscesses, burn wound sepsis, meningitis, urinary tract infections, and various nosocomial infections, in immunocompromised patients This organism holds a certain clinical relevance as it is resistant to multiple antibiotics. Using a variety of comprehensive investigations, we demonstrate that characterize the biofilm formation, microbial invasion, and tissue destruction in mono-species and dual-species infections on commercial reconstructed human oral epithelia
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