Virulence and pathogenicity ofCandida albicansis enhanced in biofilms containing oral bacteria

Cavalcanti, Yuri Wanderley; Morse, Daniel; Silva, Wander José da; Cury, Altair Antoninha Del Bel; Wei, Xiaoqinq; Wilson, Matthew; Milward, Paul J.; Lewis, Michael Alexander Oxenham; Bradshaw, David J.; Williams, David Wynne

doi:10.1080/08927014.2014.996143

Cited by 83 publications

(84 citation statements)

References 46 publications

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“…Similar enhancement of fungal burden and invasion is seen in murine C. albicans-bacterial coinfection and epithelial disease models (56)(57)(58)(59)(60).…”

Section: Discussionsupporting

confidence: 49%

Candida albicans and Pseudomonas aeruginosa Interact To Enhance Virulence of Mucosal Infection in Transparent Zebrafish

et al. 2017

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Polymicrobial infections often include both fungi and bacteria and can complicate patient treatment and resolution of infection. Cross-kingdom interactions among bacteria, fungi, and/or the immune system during infection can enhance or block virulence mechanisms and influence disease progression. The fungus Candida albicans and the bacterium Pseudomonas aeruginosa are coisolated in the context of polymicrobial infection at a variety of sites throughout the body, including mucosal tissues such as the lung. In vitro, C. albicans and P. aeruginosa have a bidirectional and largely antagonistic relationship. Their interactions in vivo remain poorly understood, specifically regarding host responses in mediating infection. In this study, we examine trikingdom interactions using a transparent juvenile zebrafish to model mucosal lung infection and show that C. albicans and P. aeruginosa are synergistically virulent. We find that high C. albicans burden, fungal epithelial invasion, swimbladder edema, and epithelial extrusion events serve as predictive factors for mortality in our infection model. Longitudinal analyses of fungal, bacterial, and immune dynamics during coinfection suggest that enhanced morbidity is associated with exacerbated C. albicans pathogenesis and elevated inflammation. The P. aeruginosa quorum-sensingdeficient ΔlasR mutant also enhances C. albicans pathogenicity in coinfection and induces extrusion of the swimbladder. Together, these observations suggest that C. albicans-P. aeruginosa cross talk in vivo can benefit both organisms to the detriment of the host.

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“…Similar enhancement of fungal burden and invasion is seen in murine C. albicans-bacterial coinfection and epithelial disease models (56)(57)(58)(59)(60).…”

Section: Discussionsupporting

confidence: 49%

Candida albicans and Pseudomonas aeruginosa Interact To Enhance Virulence of Mucosal Infection in Transparent Zebrafish

et al. 2017

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“…It has also been demonstrated that glycosyltransferase B from S. mutans-upregulated genes are involved with morphogenesis and adhesion (HWP1, ALS1, and ALS3) of C. albicans [Ellepola et al, 2017]. In mono-species biofilms of C. albicans, morphogenesis is probably due to neutral pH, whilst morphogenesis observed in dual-species biofilms may be related to sugar starvation and direct bacterial interaction [Morales and Hogan, 2010;Diaz et al, 2012;Cavalcanti et al, 2015]. The activation of morphogenesis in dual-species biofilms may favor the adhesion of C. albicans, as well as promote a greater cell-wall surface for interaction with S. mutans cells.…”

Section: Discussionmentioning

confidence: 99%

Candida albicans Increases Dentine Demineralization Provoked by Streptococcus mutans Biofilm

et al. 2018

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Streptococcus mutans are considered the most cariogenic bacteria, but it has been suggested that Candida albicans could increase their cariogenicity. However, the effect of this dual-species microorganisms’ combination on dentine caries has not been experimentally evaluated. Biofilms of C. albicans, S. mutans and C. albicans + S. mutans (n = 12/biofilm) were grown in ultra-filtered tryptone yeast extract broth culture medium for 96 h on root dentine slabs of known surface hardness and exposed 8 times per day for 3 min to 10% sucrose. The medium was changed 2 times per day (after the 8 cariogenic challenges and after the overnight period of famine), and aliquots were analyzed to determinate the pH (indicator of biofilm acidogenicity). After 96 h, the biofilms were collected to determine the wet weight, colony-forming units, and the amounts of extracellular polysaccharides (soluble and insoluble). Dentine demineralization was assessed by surface hardness loss (% SHL). The architecture of the biofilms was analyzed by confocal laser scanning microscopy (CLSM) and transmission electron microscopy (TEM). Data were analyzed by ANOVA followed by Tukey’s test (α = 0.05). The dual-species C. albicans + S. mutans biofilm provoked higher % SHL on dentine (p < 0.05) than the S. mutans and C. albicans biofilm. This was supported by the results of biofilm acidogenicity and the amounts of soluble (6.4 ± 2.14 vs. 4.0 ± 0.94 and 1.9 ± 0.97, respectively) and insoluble extracellular polysaccharides (24.9 ± 9.22 vs. 18.9 ± 5.92 and 0.7 ± 0.48, respectively) (p < 0.05). The C. albicans biofilm alone presented low cariogenicity. The images by CLSM and TEM, respectively, suggest that the C. albicans + S. mutans biofilm is more voluminous than the S. mutans biofilm, and S. mutans cells interact with C. albicans throughout polysaccharides from the biofilm matrix. These findings show that C. albicans enhances the cariogenic potential of the S. mutans biofilm, increasing dentine demineralization.

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“…Biofilms render the organisms resistant to antimicrobial agents and protect them from immune cells (13–15). Moreover, fungal filamentation is a known Candida virulence factor that damages host tissues and triggers specific host immune responses (16–19). Distinct interspecies interactions in this biofilm environment were clearly evident, where E. coli tended to be closely associated with the fungal cell walls, while S. marcescens used its fimbriae to form a “bridge” between C. tropicalis and E. coli that stabilized the bacterium-fungus biofilm structure.…”

Section: Commentarymentioning

confidence: 99%

Cooperative Evolutionary Strategy between the Bacteriome and Mycobiome

Ghannoum

2016

mBio

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Nonhealing chronic wounds are all unique in origin and circumstance, and attempting to isolate a single etiology for the failure of a wound to heal is daunting. Wounds represent complex systems of multispecies fungal and bacterial biofilms. The survival strategies of interactive microbial communities have led to cooperative evolutionary strategies that culminate in biofilm formation. In microbial dysbiosis, biofilms are beneficial to both bacterial and fungal communities but detrimental to the host. Fungi benefit by a surge in their virulence factors, while bacteria become tolerant to antibacterials as a consequence of living under the protective umbrella of the biofilm matrix. This interkingdom cooperation negatively impacts the host, as the fungi and bacteria produce extracellular enzymes that inflict tissue damage, leading to an increase in proinflammatory cytokines, which results in oxidative damage and apoptotic cell death.

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Virulence and pathogenicity ofCandida albicansis enhanced in biofilms containing oral bacteria

Cited by 83 publications

References 46 publications

Candida albicans and Pseudomonas aeruginosa Interact To Enhance Virulence of Mucosal Infection in Transparent Zebrafish

Candida albicans and Pseudomonas aeruginosa Interact To Enhance Virulence of Mucosal Infection in Transparent Zebrafish

<b><i>Candida albicans</i></b> Increases Dentine Demineralization Provoked by<b><i> Streptococcus mutans</i></b> Biofilm

Cooperative Evolutionary Strategy between the Bacteriome and Mycobiome

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