The induction of immunogenic cell death by photodynamic therapy in B16F10 cells in vitro is effected by the concentration of the photosensitizer.

Photodynamic therapy (PDT) can trigger immune responses against cancer cells. The induction of immunogenic cell death (ICD) is one of the possible mechanisms behind this event, but the protocol conditions necessary for a robust induction of ICD by PDT have not been defined. In this work, the immunogenicity of B16F10 melanoma cells treated with different PDT protocols was investigated. The exposure of damage-associated molecules (DAMPs), namely HMGB1, calreticulin and ATP, a hallmark of ICD, and the presence of apoptotic and necrotic cells were assessed after the application of PDT mediated by different concentrations of aluminum-phthalocyanine (AlPcNE) in vitro. Furthermore, the in vivo immunogenicity of PDT-treated B16F10 cells was investigated with an immunization-challenge model in C57BL/6 mice. The percentage of dead cells was directly proportional to the concentration of AlPcNE. The IC50, IC70 and IC90 concentrations of AlPcNE induced the exposure of DAMPs by B16F10 cells after PDT. In the in vivo model, however, only the B16F10 cells treated with PDT-AlPcNE at the IC50 or IC70 rendered C57BL/6 significantly more resistant to a subsequent challenge with viable B16F10 cells. Thus, the induction of ICD in B16F10 cells by PDT occurs only at a specific range of AlPcNE concentrations.

Photodynamic therapy inhibits cell growth and enhances the histone deacetylase-mediated viability impairment in Cryptococcus spp. in vitro.

Cryptococcosis is a disseminated infection caused mainly by C. neoformans and C. gattii. Limitations for the treatment involve the selection of isolates resistant to conventional antifungal drugs, prolonged treatment time and drugs side effects. This study evaluated the combined effect of histone deacetylase inhibitors (HDACi) and photodynamic therapy (PDT) on the growth of C. neoformans and C. gattii in vitro. Results showed that PDT inhibited yeasts proliferation and enhanced the HDACi-mediated cell viability impairment in Cryptococcus spp.