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Review
. 2018 Dec 13;14(12):e1007342.
doi: 10.1371/journal.ppat.1007342. eCollection 2018 Dec.

Candida-streptococcal interactions in biofilm-associated oral diseases

Hyun Koo  1 , David R Andes  2   3 , Damian J Krysan  4   5
Affiliations
Review

Candida-streptococcal interactions in biofilm-associated oral diseases

Hyun Koo et al. PLoS Pathog. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Candida–streptococcal interactions and oral diseases.
A. Confocal fluorescence microscopy images of C. albicans–S. mutans mixed biofilms, illustrating the spatial relationship between C. albicans (blue), S. mutans (green), and exopolysaccharides (red). B. Images of teeth from rats infected with S. mutans, C. albicans, or coinfected. Black arrows indicate severe carious lesions of coinfections in which enamel is missing, which exposes underlying dentin. Such rampant caries was absent in the animals infected by S. mutans or C. albicans alone. C. Fluorescence microscopy images of harvested mouse tongues infected with S. oralis (red, see arrows), C. albicans (green), or both. Coinfection substantially increased bacterial–fungal biofilm accumulation, soft tissue invasion, and inflammatory response. Original images provided by Dr. Anna Dongari-Bagtzoglou; adapted from Sobue T. and colleagues, Methods Mol Biol. 1356:137–52, 2016, with permission. EPS, exopolysaccharides.
Fig 2
Fig 2. Pathogenic mechanisms of C. albicans–oral streptococcal cross-kingdom interactions.
Complex physical and chemical interactions (including cross-feeding and metabolites exchange) as well as environmental and host factors govern the development of pathogenic bacterial–fungal biofilms, including spatial organization, virulence, and drug protection/resistance. These interactions can be cooperative or competitive to mediate symbiotic, antagonistic, or synergistic relationships, often modulated by host and environmental factors to promote the onset and amplify the severity of the disease. Host diet (dietary sugars, particularly sucrose) promote the interactions between C. albicans and S. mutans by providing a substrate for EPS α-glucans production by streptococcal Gtfs that enhances coadhesion and bacterial–fungal tooth colonization, stimulating cross-kingdom biofilms. This interaction enhances the carriage of the cariogenic pathogen and acid production, while the presence of C. albicans increases EPS matrix production (via Gtf induction and fungal-derived EPS) and biofilm aciduricity, resulting in cariogenic conditions on tooth surface. Likewise, the pathogenic impact of C. albicans interactions with MGS on mucosal surfaces is also influenced by host factors. The interactions of S. oralis with C. albicans on mucosal surfaces cause exacerbated inflammatory responses and increased neutrophilic activity. C. albicans increase the biomass of S. oralis and this leads to increased mucosal TLR2 expression, activating proinflammatory signaling. C. albicans and S. oralis also synergistically increase epithelial μ-calpain activity, a proteolytic enzyme that targets E-cadherin from epithelial junctions. The bacteria influence fungal physiology by promoting hyphal formation via the Efg1 filamentation pathway and expression of secreted aspartyl proteases, which further induces proteolytic degradation of E-cadherin, facilitating invasion and tissue destruction. Efg1; EPS, exopolysaccharides; Gtf, glucosyltransferase; MGS, mitis group streptococci; TLR2.
See this image and copyright information in PMC

References

    1. Marsh PD, Zaura E. Dental biofilm: ecological interactions in health and disease. J Clin Periodontol. 2017;44: S12–S22. 10.1111/jcpe.12679 - DOI - PubMed
    1. Peleg AY, Hogan DA, Mylonakis E. Medically important bacterial–fungal interactions. Nat Rev Microbiol. 2010;8: 340–349. 10.1038/nrmicro2313 - DOI - PubMed
    1. Harriott MM, Noverr MC. Importance of Candida–bacterial polymicrobial biofilms in disease. Trends Microbiol. 2011;19: 557–563. 10.1016/j.tim.2011.07.004 - DOI - PMC - PubMed
    1. Lohse MB, Gulati M, Johnson AD, Nobile CJ. Development and regulation of single- and multi-species Candida albicans biofilms. Nat Rev Microbiol. 2018;16: 19–31. 10.1038/nrmicro.2017.107 - DOI - PMC - PubMed
    1. Bowen WH, Burne RA, Wu H, Koo H. Oral Biofilms: Pathogens, Matrix, and Polymicrobial Interactions in Microenvironments. Trends Microbiol. 2018;26: 229–242. 10.1016/j.tim.2017.09.008 - DOI - PMC - PubMed

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