Streptococcus dentisani inhibits the growth of Candida albicans and Candida glabrata: in vitro assay.

BACKGROUND: Probiotic bacteria inhibit aggregation, biofilm formation, and dimorphism of Candida spp. However, the effects of a new probiotic, Streptococcus dentisani, on the growth of Candida albicans and Candida glabrata biofilms are unknown. OBJECTIVE: To determine the effect of S. dentisani on the different phases of C. albicans and C. glabrata biofilm development. METHODS: Growth quantification and ultrastructural analyses were performed on biofilms of C. albicans ATCC 90028, C. glabrata ATCC 2001, and clinical isolates of C. albicans from oral candidiasis (CA-C1), caries (CA-CR1), and periodontal pocket (CA-P1) treated with cell suspensions of S. dentisani CECT 7746. Cell viability was determined by quantifying colony-forming units (CFU/mL). The ultrastructural analyses were done with atomic force microscopy. RESULTS: S. dentisani induced a significant reduction (p < 0.05) of CFU/mL of immature and mature biofilm in all strains of C. albicans and C. glabrata. Microscopic analysis revealed that S. dentisani reduced C. albicans density in mixed biofilm. The fungus-bacteria interaction affected cell membrane integrity in yeast. CONCLUSION: For the first time, our data elucidate the antifungal effect of S. dentisani on the development of C. albicans and C. glabrata biofilms, supporting its usefulness as a niche-specific probiotic to prevent and treat oral dysbiosis.

Ligand Diffusion Enables Force-Independent Cell Adhesion via Activating α5ß1 Integrin and Initiating Rac and RhoA Signaling.

Cells reside in a dynamic microenvironment in which adhesive ligand availability, density, and diffusivity are key factors regulating cellular behavior. Here, the cellular response to integrin-binding ligand dynamics by directly controlling ligand diffusivity via tunable ligand-surface interactions is investigated. Interestingly, cell spread on the surfaces with fast ligand diffusion is independent of myosin-based force generation. Fast ligand diffusion enhances α5ß1 but not αvß3 integrin activation and initiates Rac and RhoA but not ROCK signaling, resulting in lamellipodium-based fast cell spreading. Meanwhile, on surfaces with immobile ligands, αvß3 and α5ß1 integrins synergistically initiate intracellular-force-based canonical mechanotransduction pathways to enhance cell adhesion and osteogenic differentiation of stem cells. These results indicate the presence of heretofore-unrecognized pathways, distinct from canonical actomyosin-driven mechanisms, that are capable of promoting cell adhesion.