Correction: In vivo evaluation of photodynamic inactivation using Photodithazine® against Candida albicans.

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.

In vivo photodynamic inactivation of Candida albicans using chloro-aluminum phthalocyanine.

This study evaluated the photoinactivation of Candida albicans in a murine model of oral candidiasis using chloro-aluminum phthalocyanine (ClAlP) encapsulated in cationic nanoemulsions (NE) and chloro-aluminum phthalocyanine (ClAlP) diluted in DMSO (DMSO) as photosensitizer (PS). Seventy-five 6-week-old female Swiss mice were immunosuppressed and inoculated with C. albicans to induce oral candidiasis. PDT was performed on the tongue by the application of the photosensitizers and LED light (100 J cm(-2) -660 nm). Twenty-four hours and 7 days after treatments, microbiological evaluation was carried out by recovering C. albicans from the tongue of animals (CFU ml(-1) ). Then, mice were sacrificed and the tongues were surgically removed for histological and biomolecular analysis of pro- and anti-inflammatory cytokines. Data were analyzed by ANOVA followed by Tukey's post hoc test. ClAlP-NE-mediated PDT reduced 2.26 log10 of C. albicans recovered from the tongue when compared with the control group (P-L-) (P < 0.05). PDT did not promote adverse effects on the tongue tissue. Seven days after treatment, all animals were completely healthy. In summary, PDT mediated by chloro-aluminum phthalocyanine entrapped in cationic nanoemulsions was effective in reducing C. albicans recovered from the oral lesions of immunocompromised mice.

In vivo evaluation of photodynamic inactivation using Photodithazine® against Candida albicans.

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.

Photodynamic inactivation of clinical isolates of Candida using Photodithazine®.

This study evaluated the photodynamic inactivation (PDI) mediated by Photodithazine(®) (PDZ) against 15 clinical isolates of Candida albicans, Candida glabrata and Candida tropicalis. Each isolate, in planktonic and biofilm form, was exposed to PDI by assessing a range of PDZ concentrations and light emitting diode fluences. Cell survival of the planktonic suspensions was determined by colony forming units (CFU ml(-1)). The antifungal effects of PDI against biofilms were evaluated by CFU ml(-1) and metabolic assay. Data were analyzed by non-parametric tests (α = 0.05). Regardless of the species, PDI promoted a significant viability reduction of planktonic yeasts. The highest reduction in cell viability of the biofilms was equivalent to 0.9 log10 (CFU ml(-1)) for C. albicans, while 1.4 and 1.5 log10 reductions were obtained for C. tropicalis and C. glabrata, respectively. PDI reduced the metabolic activity of biofilms by 62.1, 76.0, and 76.9% for C. albicans, C. tropicalis, and C. glabrata, respectively. PDZ-mediated PDI promoted significant reduction in the viability of Candida isolates.

Comparison of Photodynamic Therapy versus conventional antifungal therapy for the treatment of denture stomatitis: a randomized clinical trial.

In this randomized clinical trial, the clinical and mycological efficacy of Photodynamic Therapy (PDT) was compared with that of topical antifungal therapy for the treatment of denture stomatitis (DS) and the prevalence of Candida species was identified. Patients were randomly assigned to one of two groups (n = 20 each); in the nystatin (NYT) group patients received topical treatment with nystatin (100,000 IU) four times daily for 15 days and in the PDT group the denture and palate of patients were sprayed with 500 mg/L of Photogem(®), and after 30 min of incubation, were illuminated by light emitting-diode light at 455 nm (37.5 and 122 J/cm(2), respectively) three times a week for 15 days. Mycological cultures taken from dentures and palates and standard photographs of the palates were taken at baseline (day 0), at the end of the treatment (day 15) and at the follow-up time intervals (days 30, 60 and 90). Colonies were quantified (CFU/mL) and identified by biochemical tests. Data were analysed by Fisher's exact test, analysis of variance and Tukey tests and κ test (α = 0.05). Both treatments significantly reduced the CFU/mL at the end of the treatments and on day 30 of the follow-up period (p <0.05). The NYT and PDT groups showed clinical success rates of 53% and 45%, respectively. Candida albicans was the most prevalent species identified. PDT was as effective as topical nystatin in the treatment of DS.

Susceptibility of Staphylococcus aureus to porphyrin-mediated photodynamic antimicrobial chemotherapy: an in vitro study.

The ability of Staphylococcus aureus to develop multidrug resistance is well documented, and the antibiotic resistance showed by an increasing number of bacteria has shown the need for alternative therapies to treat infections, photodynamic therapy (PDT) being a potential candidate. The aim of this study was to determine the effect of photodynamic therapy as a light-based bactericidal modality to eliminate Staphylococcus aureus. The study investigated a technique based on a combination of light and a photosensitizer that is capable of producing oxidative species to induce a cytotoxic effect. A Staphylococcus aureus suspension was exposed to a light emitting diode (LED) emitting at 628 nm, 14.6 mW/cm(2), and energy density of 20 J/cm(2), 40 J/cm(2), or 60 J/cm(2) in the presence of different porphyrin concentrations (Photogem). Three drug concentrations were employed: 12 microl/ml, 25 microl/ml, and 50 microl/ml. The treatment response was evaluated by the number of bacterial colony forming units (CFU) after light exposure. The results indicated that exposure to 60 J/cm(2) eliminated 100% (10 log(10) scales) of bacteria, on average. The best PDT response rate to eliminate Staphylococcus aureus was achieved with exposure to LED light in combination with the photosensitizer at concentrations ranging from 25 microl/ml to 50 microl/ml. These data suggest that PDT has the potential to eliminate Staphylococcus aureus in suspension and indicates the necessary drug concentration and light fluency.

Effects of angiotensin and vasopressin V(1) receptors on water and sodium intake induced by injection of vasopressin into lateral septal area.

The specific arginine(8)-vasopressin (AVP) V(1) receptors antagonist (AAVP) was injected (20, 40 and 80 nmol) into the lateral septal area (LSA) to determine the effects of selective septal V(1) receptor on water and 3% sodium intake in rats. Was also observed the effects of losartan and CGP42112A (select ligands of the AT(1) and AT(2) ANG II receptors, respectively) injected into LSA prior AVP on the same appetites. Twenty-four hours before the experiments, the rats were deprived of water. The volume of drug solution injected was 0.5 microl. Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Injection of AVP reduced the water and sodium ingestion vs. control (0.15 M saline). Pre-treatment with AAVP (40, 80 and 160 nmol) did not alter the decrease in the water ingestion induced by AVP, whereas AAVP abolished the action of AVP-induced sodium intake. Losartan (40, 80 and 160 nmol) did not alter the effect of AVP on water and sodium intake, whereas CGP42112A (20, 40 and 60 nmol) at the first 30 min increased water ingestion. Losartan and CGP42112A together increased the actions of AVP, showing more pronounced effects than when the two antagonists were injected alone. The results showed that AVP inhibited the appetites and these effects were increased by the AAVP. The involvement of angiotensinergic receptors in the effects of AVP is also suggested.