Development of an antimicrobial fungal egg tray containing orange oil and smoke for eggs preservation at room temperature

ABSTRACT: The prevention and controlled growth of pathogenic bacteria on eggs during storage and distribution at room temperature is important to ensure commercial eggs and egg products are safe for consumer. This study investigated the combined effects of orange oil (0.001%–0.004% v/w) and smoke for 10 min in paper egg tray packaging produce from the fungal pulp of Trametes versicolor. Eggs were kept in the developed paper egg tray at room temperature (30 ± 2°C). The mechanism of the combined antibacterial effects against Escherichia coli, Salmonella Typhimurium, and Staphylococcus aureus and egg quality were investigated. The combination of orange oil (0.004%) and smoke delayed all bacteria and suppressed changes in weight loss and the quality factor of eggs (Haugh unit, yolk index, albumen index) for at least 14 d. It was found that the volatile orange oil smoke in the egg tray could be passed through the structure of the cell wall and membrane of bacteria, giving rise to loss of cell viability by irreversibly damaging the cell membranes of all the bacteria in this test. Moreover, higher antioxidant activity was found on the eggs than on the eggshells, which is linked to greater shelf-life of treated eggs. The study demonstrates an improved paper egg tray packaging system and the possibility of combining released essential oils and smoke, which can be extended to egg products. Smoke can also be modified on the surface of paper egg trays easily, which shows potential in functionalizing implanted materials with antibacterial properties

STAT3-dependent VEGF production from keratinocytes abrogates dendritic cell activation and migration by arsenic: a plausible regional mechanism of immunosuppression in arsenical cancers

[[abstract]]Arsenic remains an important environmental hazard that causes several human cancers. Arsenic-induced Bowen’s disease (As-BD), a skin carcinoma in situ, is the most common arsenical cancer. While great strides have been made in our understanding of arsenic carcinogenesis, how host immunity contributes to this process remains unknown. Patients with As-BD have an impaired contact hypersensitivity response. Although impaired T cell activation has been well-documented in arsenical cancers, how dendritic cell (DC), the key cell regulating innate immunity, regulates the immune response in arsenical cancers remains unclear. Using myeloid derived DC (MDDC) from patients with As-BD and normal controls as well as bone marrow derived DC (BMDC) from mice fed with or without arsenic, we measured the migration of DC. As-BD patients showed an impaired CCL21-mediated MDDC migration in vitro. Arsenic-fed mice had defective DC migration towards popliteal lymph nodes when injected with allogenic BMDCs via foot pad. Using skin from As-BD and normal controls, we found an increased expression of STAT3, a transcriptional factor contributing to impaired DC activation. Arsenic induced STAT3 activation and the production of VEGF in keratinocytes. The increase in VEGF was blocked by inhibiting STAT3 with RNA interference or pharmaceutically with JSI-124. While VEGF by itself minimally induced the expression of CD86 and MHC-II in MDDC, arsenic induced-MDDC activation was abolished by VEGF pretreatment. We concluded that the STAT3-VEGF axis in keratinocytes inhibits DC migration in the microenvironment of As-BD, indicating that cellular interactions play an important role in regulating the disease course of arsenical cancers