• Riboflavin demonstrates antioxidant and photosensitizing properties. • Riboflavin is able to induce ROS and modulate immune response. • Riboflavin possesses potent antimicrobial activity when used alone or combined with other anti-infectives. • The riboflavin biosynthesis pathway serves as an ideal drug target against microbes. • UVA combination with riboflavin exhibits remarkable antimicrobial effects.

Candida bloodstream infections remain the most frequent life-threatening fungal disease, with Candida albicans accounting for 70% to 80% of the Candida isolates recovered from infected patients. In nature, Candida species are part of the normal commensal flora in mammalian hosts. However, they can transform into pathogens once the host immune system is weakened or breached. More recently, mortality attributed to Candida infections has continued to increase due to both inherent and acquired drug resistance in Candida, the inefficacy of the available antifungal drugs, tedious diagnostic procedures, and a rising number of immunocompromised patients. Adoption of animal models, viz. minihosts, mice, and zebrafish, has brought us closer to unraveling the pathogenesis and complexity of Candida infection in human hosts, leading towards the discovery of biomarkers and identification of potential therapeutic agents. In addition, the advancement of omics technologies offers a holistic view of the Candida-host interaction in a non-targeted and non-biased manner. Hence, in this review, we seek to summarize past and present milestone findings on C. albicans virulence, adoption of animal models in the study of C. albicans infection, and the application of omics technologies in the study of Candida–host interaction. A profound understanding of the interaction between host defense and pathogenesis is imperative for better design of novel immunotherapeutic strategies in future.

Silver nanoparticles (AgNPs) are commonly used in numerous consumer products, including textiles, cosmetics, and health care items. The widespread usage of AgNPs results in their unavoidable discharge into the ecosystem, which pollutes the aquatic, groundwater, sediments, and marine environments. These nanoparticles (NPs) activate the production of free radicals reactive species in aquatic organisms that interrupt the functions of DNA, cause mitochondrial dysfunction, and increase lipid peroxidation, which terminates the development and reproduction both in vivo and in vitro. The life present in the aquatic ecosystem is becoming threatened due to the release and exploitation of AgNPs. Managing the aquatic ecosystem from the AgNP effects in the near future is highly recommended. In this review, we discussed the background of AgNPs, their discharge, and uptake by aquatic organisms, the mechanism of toxicity, different pathways of cytotoxicity, and bioaccumulation, particularly in aquatic organisms. We have also discussed the antimicrobial activities of AgNPs along with acute and chronic toxicity in aquatic groups of organisms.

The recently identified cytokines—interleukin (IL)-35 and interleukin (IL)-37—have been described for their anti-inflammatory and immune-modulating actions in numerous inflammatory diseases, auto-immune disorders, malignancies, infectious diseases and sepsis. Either cytokine has been reported to be reduced and in some cases elevated and consequently contributed towards disease pathogenesis. In view of the recent advances in utilizing cytokine profiles for the development of biological macromolecules, beneficial in the management of certain intractable immune-mediated disorders, these recently characterized cytokines (IL-35 and IL-37) offer potential as reasonable targets for the discovery of novel immune-modulating anti-inflammatory therapies. A detailed comprehension of their sophisticated regulatory mechanisms and patterns of expression may provide unique opportunities for clinical application as highly selective and target specific therapeutic agents. This review seeks to summarize the recent advancements in discerning the dynamics, mechanisms, immunoregulatory and anti-inflammatory actions of IL-35 and IL-37 as they relate to disease pathogenesis.