Abstract
Objective: The aim of this study was evaluate the effect of Bacillus subtilis on Candida albicans biofilm formation and filamentation by evaluating the gene expression of ALS3, HWP1, BCR1, EFG1 and TEC1. Material and Methods: Mixed (C. albicans / B.subtilis) and monotypic biofilms were cultured in plates at 37°C for 48 h under shaking for counting viable cells (CFU / mL) and analysis of gene expression by real-time PCR. The C. albicans filamentation assay was performed in medium containing 10% fetal bovine serum at 37°C for 6 hours. Data was analysed by t-Student and Mann– Whitney tests. Results: B. subtilis reduced the biofilm formation of C. albicans in 1 log when cultured in the same environment (p<0.0001). In addition, it significantly reduced the yeast -hypha transition affecting the morphology of C. albicans. Among all of the analyzed genes, the ALS3 and HWP1 genes were the most affected, achieving 111.1- and 333.3- fold decreases in the C. albicans biofilms associated with B. subtilis, respectively. Conclusion: B. subtilis reduced the biofilm formation and filamentation of C. albicans by negatively regulating the ALS3, HWP1, BCR1, EFG1 and TEC1 genes that are essential for the production of biofilm and hyphae.KeywordsBacillus subtilis; Candida albicans; Biofilm; Filamentation; Gene expression.
Highlights
Candida albicans is a commensal fungus found on mucosal surfaces of the oral cavity, gastrointestinal and genitourinary tracts
B. subtilis reduced the biofilm formation and filamentation of C. albicans by negatively regulating the ALS3, HWP1, BCR1, EFG1 and TEC1 genes that are essential for the production of biofilm and hyphae
The CFU/mL count of C. albicans in monotypic biofilms showed higher values compared to mixed biofilms formed by associations between C. albicans and B. subtilis (Figure 1)
Summary
Candida albicans is a commensal fungus found on mucosal surfaces of the oral cavity, gastrointestinal and genitourinary tracts. This yeast causes severe and recurrent mucosal infections as well as fatal invasive infections in both immunocompromised and immunocompetent individuals [1]. Some virulence factors such as dimorphism and the ability to adhere and form biofilm on medical devices and/or the host mucosal epithelium, enhance the pathogenicity of C. albicans. Advances in genetic manipulation and expression profiling have helped define the regulatory pathways and mechanisms that govern C. albicans biofilm development [1,2,3]. Several classes of genes, such as specify transcription factors (EFG1, BCR1, TEC1) and adhesion (HWP1, ALS3), control biofilm development on abiotic and biotic surfaces [4,5]
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