Candida albicans biofilm development is governed by cooperative attachment and adhesion maintenance proteins

McCall, Andrew D.; Pathirana, Ruvini U.; Prabhakar, Aditi; Cullen, Paul J.; Edgerton, Mira

doi:10.1038/s41522-019-0094-5

Cited by 89 publications

(67 citation statements)

References 33 publications

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“…In Salmonella, biofilm-associated protein, BapA, is an important structural component for biofilm formation, and calcium was found to be important for proper protein folding (Guttula et al, 2019). In addition, biofilm-associated surface proteins are important for the maintenance of biofilm (McCall et al, 2019). Fourth, calcium can function as a signal and induce the expression of genes involved in different pathways to mediate biofilm formation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Calcium and Signal Sensing Systems on Azorhizobium caulinodans Biofilm Formation and Host Colonization

et al. 2020

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Biofilm formation is important for establishing plants-microbe associations. The role of calcium on biofilm formation has been studied in many bacteria except rhizobia. In this study, we investigated the role of calcium for biofilm formation in Azorhizobium caulindans, which forms nodules in the stem and root of its host plant Sesbania rostrata. We found that calcium is essential for A. caulindans biofilm formation, in addition to the presence of extracellular matrix components, eDNA and proteins. Also, calcium-mediated biofilm formation was tested with chemotaxis, motility, cyclic di-GMP synthesis, and quorum sensing mutants. Finally, calcium was found to promote S. rostrata root colonization of A. caulinodans. In total, these results show that calcium is essential for A. caulindans biofilm formation, and it affects the interaction between A. caulinodans and host plant.

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Section: Discussionmentioning

confidence: 99%

Effects of Calcium and Signal Sensing Systems on Azorhizobium caulinodans Biofilm Formation and Host Colonization

et al. 2020

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“…On the other hand, the YWP1 gene was upregulated with SM-F2 treatment. YWP1 (Yeast Wall protein 1) is an anchored glycoprotein of the cell wall present only in the yeast form, absent in filamentous form and chlamydospores (Granger, 2012;McCall et al, 2019). Therefore, these results suggest that the activity of SM-F2 against filamentation observed in the microscopic analysis can be associated with the level of transcription in C. albicans cells that leads to retention in the yeast state.…”

Section: Discussionmentioning

confidence: 78%

Streptococcus mutans Secreted Products Inhibit Candida albicans Induced Oral Candidiasis

et al. 2020

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In the oral cavity, Candida species form mixed biofilms with Streptococcus mutans, a pathogenic bacterium that can secrete quorum sensing molecules with antifungal activity. In this study, we extracted and fractioned culture filtrate of S. mutans, seeking antifungal agents capable of inhibiting the biofilms, filamentation, and candidiasis by Candida albicans. Active S. mutans UA159 supernatant filtrate components were extracted via liquid-liquid partition and fractionated on a C-18 silica column to resolve S. mutans fraction 1 (SM-F1) and fraction 2 (SM-F2). We found anti-biofilm activity for both SM-F1 and SM-F2 in a dose dependent manner and fungal growth was reduced by 2.59 and 5.98 log for SM-F1 and SM-F2, respectively. The SM-F1 and SM-F2 fractions were also capable of reducing C. albicans filamentation, however statistically significant differences were only observed for the SM-F2 (p = 0.004). SM-F2 efficacy to inhibit C. albicans was confirmed by its capacity to downregulate filamentation genes CPH1, EFG1, HWP1, and UME6. Using Galleria mellonella as an invertebrate infection model, therapeutic treatment with SM-F2 prolonged larvae survival. Examination of the antifungal capacity was extended to a murine model of oral candidiasis that exhibited a reduction in C. albicans colonization (CFU/mL) in the oral cavity when treated with SM-F1 (2.46 log) and SM-F2 (2.34 log) compared to the control (3.25 log). Although both SM-F1 and SM-F2 fractions decreased candidiasis in mice, only SM-F2 exhibited significant quantitative differences compared to the non-treated group for macroscopic lesions, hyphae invasion, tissue lesions, and inflammatory infiltrate. Taken together, these results indicate that the SM-F2 fraction contains antifungal components, providing a promising resource in the discovery of new inhibitors for oral candidiasis.

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“…The Dongari-Bagtzoglou group previously showed that the presence of oral streptococci increases the ability of C. albicans to invade organotypic models of oral mucosa ( 9 ) and that Streptococcus oralis can activate C. albicans EFG1 gene expression (a key inducer of hyphae and microcolonies) that increases polymicrobial biofilm ( 52 ). In addition, coinfections of S. oralis and C. albicans increase mucosal fungal invasion ( 53 ), and coculture of C. albicans with S. gordonii induces the expression of fungal filamentation genes and hyphal adhesins, including Als1, Hyr1, and Eap1 ( 11 ), some of which we showed are important for microcolony adhesion ( 54 ). However, we found that S. gordonii supernatants induced a dual phenotype, with the majority of C. albicans microcolonies becoming enlarged and detached from an underlying epithelium, while some microcolonies (30%) had less biomass but were highly invasive.…”

Section: Discussionmentioning

confidence: 92%

Bacteria Modify Candida albicans Hypha Formation, Microcolony Properties, and Survival within Macrophages

Salvatori

Kumar

Metcalfe

et al. 2020

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Phagocytic cells are crucial components of the innate immune system preventing Candida albicans mucosal infections. Streptococcus gordonii and Pseudomonas aeruginosa often colonize mucosal sites, along with C. albicans, and yet interkingdom interactions that might alter the survival and escape of fungi from macrophages are not understood. Murine macrophages were coinfected with S. gordonii or P. aeruginosa, along with C. albicans to evaluate changes in fungal survival. S. gordonii increased C. albicans survival and filamentation within macrophage phagosomes, while P. aeruginosa reduced fungal survival and filamentation. Coinfection with S. gordonii resulted in greater escape of C. albicans from macrophages and increased size of fungal microcolonies formed on macrophage monolayers, while coinfection with P. aeruginosa reduced macrophage escape and produced smaller microcolonies. Microcolonies formed in the presence of P. aeruginosa cells outside macrophages also had significantly reduced size that was not found with P. aeruginosa phenazine deletion mutants. S. gordonii cells, as well as S. gordonii heat-fixed culture supernatants, increased C. albicans microcolony biomass but also resulted in microcolony detachment. A heat-resistant, trypsin-sensitive pheromone processed by S. gordonii Eep was needed for these effects. The majority of fungal microcolonies formed on human epithelial monolayers with S. gordonii supernatants developed as large floating structures with no detectable invasion of epithelium, along with reduced gene expression of C. albicans HYR1, EAP1, and HWP2 adhesins. However, a subset of C. albicans microcolonies was smaller and had greater epithelial invasiveness compared to microcolonies grown without S. gordonii. Thus, bacteria can alter the killing and escape of C. albicans from macrophages and contribute to changes in C. albicans pathogenicity. IMPORTANCE Candida albicans is the predominant fungus colonizing the oral cavity that can have both synergistic and antagonistic interactions with other bacteria. Interkingdom polymicrobial associations modify fungal pathogenicity and are believed to increase microbial resistance to innate immunity. However, it is not known how these interactions alter fungal survival during phagocytic killing. We demonstrated that secreted molecules of S. gordonii and P. aeruginosa alter C. albicans survival within the phagosome of macrophages and alter fungal pathogenic phenotypes, including filamentation and microcolony formation. Moreover, we provide evidence for a dual interaction between S. gordonii and C. albicans such that S. gordonii signaling peptides can promote C. albicans commensalism by decreasing microcolony attachment while increasing invasion in epithelial cells. Our results identify bacterial diffusible factors as an attractive target to modify virulence of C. albicans in polymicrobial infections.

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Candida albicans biofilm development is governed by cooperative attachment and adhesion maintenance proteins

Cited by 89 publications

References 33 publications

Effects of Calcium and Signal Sensing Systems on Azorhizobium caulinodans Biofilm Formation and Host Colonization

Effects of Calcium and Signal Sensing Systems on Azorhizobium caulinodans Biofilm Formation and Host Colonization

Streptococcus mutans Secreted Products Inhibit Candida albicans Induced Oral Candidiasis

Bacteria Modify Candida albicans Hypha Formation, Microcolony Properties, and Survival within Macrophages

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