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Correction for 'In vivo evaluation of photodynamic inactivation using Photodithazine® against Candida albicans' by J. C. Carmello, et al., Photochem. Photobiol. Sci., 2015, 14, 1319-1328.

This study evaluated the effects of antimicrobial photodynamic therapy (aPDT) mediated by Photodithazine® (PDZ) and LED light on the virulence factors of fluconazole-susceptible (CaS) and fluconazole-resistant (CaR) Candida albicans. Standardized suspensions of strains were prepared (10 7 ), and after 48 h of biofilm formation, these strains were incubated with PDZ (100 mg/L) for 20 min and exposed to LED light (660 nm, 37.5 J/cm 2 ). Additional samples were treated with PDZ or light only, and the control consisted of biofilms that received no treatment. After aPDT, the cells were recovered and the virulence factors were evaluated. To analyze the capacity of adhesion, cells were recovered after aPDT and submitted to the adhesion process in the bottom of a 96-well plate. After this, metabolic activity tests (XTT assay) and cell viability (colony forming units per milliliter, CFU/mL) were applied. To evaluate the biofilm-forming ability after aPDT, the cells recovered were submitted to biofilm formation procedures, and the biofilm formed was evaluated by XTT, CFU/mL, and total biomass (crystal violet) tests. Lastly, the capacity for synthesizing protease and phospholipase enzymes after aPDT was evaluated by fluorimetric tests. Data were analyzed by two- or three-way ANOVA tests (p ≤ 0.05). It was verified that aPDT reduced the viability of both strains, fluconazole-susceptible and fluconazole-resistant C. albicans. It was also observed that the CaR strain had lower susceptibility to the aPDT when compared with the CaS strain. However, regarding the virulence factors evaluated, it was demonstrated that aPDT did not alter the adherence and biofilm formation ability and enzymatic production.

This study evaluated the potential of curcumin-mediated antimicrobial photodynamic inactivation (API) on multispecies biofilms of Candida albicans, Candida glabrata, and Streptococcus mutans of different ages. Acrylic samples (n = 480) were made with standardized rough surfaces and incubated with bacteria and yeast for 24 or 48 h. API was performed with curcumin (80, 100, 120 μM) and LED light. Additional acrylic samples were treated with curcumin or LED light only. Positive control samples received neither light nor curcumin. After API, colony counts were quantified (CFU/mL), cell metabolism was determined by means of XTT assay, and the total biofilm biomass was evaluated using Crystal Violet (CV) staining assay and images were obtained by confocal laser scanning microscopy (CLSM). The data were analyzed by nonparametric two-way ANOVA and post hoc Tukey tests (α < 0.05). For 24-h biofilm, API resulted in statistically significant difference (ρ < 0.001) of viability of C. albicans compared with control (P-L-) for all Cur concentrations. For 48-h biofilm, API resulted in statistically significant difference (ρ < 0.001) compared with control only when Cur at 120 μM was used. API promoted statistically significant difference (ρ ≤ 0.001) in the viability of S. mutans and C. glabrata for all Cur concentrations in the two biofilm ages. In addition, API produced a statistically significant difference (ρ < 0.001) of metabolic activity and of total biomass (ρ < 0.001) of multispecies biofilms compared with control for all Cur concentrations. It can be concluded that both 24- and 48-h biofilms were susceptible to API mediated by Cur; however, 24-h biofilm was more sensitive than the 48-h biofilm.

This study assessed the cytotoxicity of antimicrobial Photodynamic Inactivation (aPDI), mediated by curcumin, using human keratinocytes co-cultured with Candida albicans. Cells and microorganisms were grown separately for 24 hours and then kept in contact for an additional 24 hours. After this period, aPDI was applied. The conditions tested were: P+L+ (experimental group aPDI); P-L+ (light emitting diode [LED] group); P+L- (curcumin group); and P-L- (cells in co-culture without curcumin nor LED). In addition, keratinocytes and C. albicans were grown separately, were not placed in the co-culture and did not receive aPDI (control group). Cell proliferation was assessed using Alamar Blue, MTT, XTT and CFU tests. Qualitative and quantitative analyses were performed. Analysis of variance (ANOVA) was applied to the survival percentages of cells compared to the control group (considered as 100% viability), complemented by multiple comparisons using Tukey's test. A 5% significance level was adopted. The results of this study showed no interference in the metabolism of the cells in co-culture, since no differences were observed between the control group (cultured cells by themselves) and the P-L- group (co-culture cells without aPDI). The aPDI group reached the highest reduction (p = 0.009), which was equivalent to 1.7 log10 when compared to the control group. The P+L-, P-L+, P-L- and control groups were not statistically different (ρ > 0.05). aPDI inhibited the growth of keratinocytes and C. albicans in all tests, so the therapy was considered slightly (inhibition between 25 and 50% compared to the control group) to moderately (inhibition between 50 and 75% compared to the control group) cytotoxic.

In this investigation, the effectiveness of successive applications of antimicrobial photodynamic inactivation (API) mediated by Photodithazine(®) (PDZ) and LED light was evaluated against a multispecies biofilm formed by Candida albicans, Candida glabrata, and Streptococcus mutans on denture base acrylic resin. Standard cell suspensions (bacteria and yeast) were inoculated on acrylic resin samples, and the biofilm was grown for 48 h (37 °C/75 rpm). API was performed by the administration of PDZ (175 and 200 mg/L) and exposure to 37.5 J/cm(2) of LED light (660 nm). Additional samples were treated with PDZ or LED light only. Untreated control samples were not submitted to light or PDZ. The conditions described were applied once or in three consecutive applications for all groups. Cell viability was determined by colony counts (CFU/mL), metabolic activity, total biomass, and confocal laser scanning microscopy (CLSM). Data were analyzed by a nonparametric two-way ANOVA and Tukey tests (α = 0.05). The results obtained demonstrated a significant effect (p < 0.05) of number of applications and treatment groups for CFU/mL, and S. mutans showed the highest susceptibility to API. The metabolic activity of the multispecies biofilm was significantly reduced (p < 0.05) after API for both numbers of applications, which were also significantly different (p < 0.05) between them. The total biomass of the biofilm was significantly different (p < 0.05) only between groups submitted to one and three API applications. CLSM showed a visual increase of dead cells after API. API-mediated PDZ was effective in reducing the cell viability of multispecies biofilm. Three consecutive applications of API were more effective for reducing the cell viability and the total biomass of multispecies biofilm.

This study describes the photoinactivation of Candida albicans in a murine model of oral candidosis, mediated by Photodithazine® (PDZ). Six-week-old female Swiss mice were immunosuppressed, and inoculated with C. albicans to induce oral candidosis. After five days, photodynamic inactivation (PDI) mediated by PDZ at concentrations of 75, 100, 125 and 150 mg L(-1) was applied on the tongue of mice. Next, microbiological evaluation was performed by recovering C. albicans from the tongue via colony forming units (CFU mL(-1)). After 24 h of treatment, the animals were killed and the tongues were surgically removed for histological analysis. PDI was effective in reducing C. albicans on the tongue of mice using 100 mg L(-1) of PDZ, when compared to the positive control group (without treatment). No adverse effect on the tongue tissue was verified after PDI. Therefore, PDI was effective for inactivation of C. albicans without causing any harmful effects on host tissues, which is promising for future clinical trials.