Melanin nanoparticles are known to be biologically benign to human cells for a wide range of concentrations in a high glucose culture nutrition. Here, we show cytotoxic behavior at high nanoparticle and low glucose concentrations, as well as at low nanoparticle concentration under exposure to (nonionizing) visible radiation. To study these effects in detail, we developed highly monodispersed melanin nanoparticles (both uncoated and glucose-coated). In order to study the effect of significant cellular uptake of these nanoparticles, we employed three cancer cell lines: VM-M3, A375 (derived from melanoma), and HeLa, all known to exhibit strong macrophagic character, i.e., strong nanoparticle uptake through phagocytic ingestion. Our main observations are: (i) metastatic VM-M3 cancer cells massively ingest melanin nanoparticles (mNPs); (ii) the observed ingestion is enhanced by coating mNPs with glucose; (iii) after a certain level of mNP ingestion, the metastatic cancer cells studied here are observed to die—glucose coating appears to slow that process; (iv) cells that accumulate mNPs are much more susceptible to killing by laser illumination than cells that do not accumulate mNPs; and (v) non-metastatic VM-NM1 cancer cells also studied in this work do not ingest the mNPs, and remain unaffected after receiving identical optical energy levels and doses. Results of this study could lead to the development of a therapy for control of metastatic stages of cancer.

Necrotizing fasciitis is a potentially fatal soft tissue infection that requires prompt clinical suspicion, pharmacological and surgical interventions. Bacterial pathogens, such as beta-hemolytic streptococcus and Staphylococcus aureus, are the main etiology of necrotizing fasciitis, however, rare cases caused by fungal pathogens, such as Candida albicans, have been reported following trauma. Here, we present the first case of C. albicans necrotizing fasciitis following an elective surgical procedure in an immunocompetent adult.

At the skin’s surface, the epidermis must balance stem cell renewal with barrier maintenance to withstand environmental stress and shield against pathogens. In this study, we identify a microbial-immune-epithelial feedback mechanism that integrates environmental information into stem cell regulation in mice. Specifically, we show that Langerhans cells (LCs), an intraepithelial macrophage population, orchestrate this circuit by producing prostaglandin E ₂ , which restrains stem cell proliferation, promotes epidermal differentiation, and maintains barrier integrity during homeostasis. Upon pathway disruption, stem cells become overactivated, hindering terminal differentiation and weakening barrier function. Upstream, LC activity is tuned by the local microbial environment in a rheostat-like fashion, coupling commensal sensing to stem cell dynamics. Our findings provide a general framework for how barrier tissues achieve adaptive homeostasis amid continual external fluctuations.