Turmeric, often called ‘the golden spice’ or ‘the spice of life’, is widely known for its culinary uses. Additionally, it has long been used medicinally to treat a wide breadth of ailments, including immune conditions and associated symptoms, and remains in use today.

Curcumin is the primary bioactive compound in turmeric. It exhibits immunomodulatory properties, yet we do not completely understand the precise pathways of modulation. Current treatments for immune conditions generally suppress immune response globally, potentially causing side effects when broad suppression interferes with normal functioning. Curcumin’s anti-inflammatory properties could provide a more targeted and preventative treatment. 

This study investigates curcumin’s  immunomodulatory mechanisms in vitro and in vivo. We utilized a dye-based exclusion assay to determine the dose-dependent toxicity/effects of curcumin-treated MC/9 mast cells and Jurkat T cells, providing data in multiple immune pathways. Mast cells release pro-inflammatory cytokines, like interleukin-1β (IL-1β), which recruit other immune cells and begin a cascading immune response. To quantify the inhibitory effects of curcumin on stimulated mast cells an enzyme linked immuno-absorbent assay measures IL-1β cytokine release. We plan to use curcumin as a topical treatment of psoriasis in mice and score clinically for reduction in symptoms, aiming to identify local and distal effects. 

Through our scientific approach, we aim to better understand curcumin’s anti-inflammatory properties and explore its therapeutic potential.

Human noroviruses are a leading cause of foodborne illnesses, yet we still lack effective and rapid disinfectants. Carvacrol, a plant-derived phenolic compound, has demonstrated antiviral activity in previous studies. However, most evidence is based on long contact times and has not been evaluated using Tulane virus, a widely accepted human norovirus surrogate. This study investigated the antiviral efficacy of carvacrol, individual surfactants (CTAB and SDS), and carvacrol-surfactant emulsions using a 5-minute suspension assay designed to mimic realistic disinfection conditions. Viral reductions were quantified using plaque assays following neutralization with 3% meat extract. 

Across all treatments, antiviral activity against Tulane virus was minimal, with log₁₀ reductions ranging from -0.509 to 0.635. No formulation achieved a meaningful reduction. Negative log reductions were attributed to normal variability in plaque enumeration when true viral inactivation is negligible. The lack of efficacy observed is likely influenced by the short contact time, the inherent recalcitrance of non-enveloped viruses, and concentration limitations due to cytotoxicity. Overall, these findings indicate that carvacrol-based emulsions and the tested surfactants, at non-cytotoxic concentrations and short exposure times, likely lack ideal efficacy as surface disinfectants against Tulane virus. Future studies should investigate longer contact times, alternative formulation strategies that reduce cytotoxicity, and improved delivery systems to better assess the antiviral potential of carvacrol for food safety and public health applications.

Neutrophils are part of our innate immune system, the body’s first line of response to disease. When activated normally, neutrophils can fight off pathogens and protect us against disease, however, in some cases, an overactive immune response can lead to inflammatory diseases. The goal of this project is to study the effects of nanoparticle composition, both lipid- and polymer-based, on nanoparticle stability and neutrophil-nanomaterial interactions. I am focusing on modulating the internalization of LNPs and PNPs and activation of the inflammatory cytokines in neutrophils. Inflammatory cytokines play a major role in inflammatory diseases such as pancreatitis, psoriasis, and arthritis. We work with both polymer nanoparticles (PNPs) and LNPs to modulate inflammatory activation for different disease models. We are using the PNPs to target activation pathways as a potential therapy for cancer and the LNPs to inhibit or reduce activation as a therapy for inflammatory diseases. I am looking at how altering their chemical composition affects their stability and their effect on neutrophils. Traditionally, we have used DSPE-PEG(2000)-carboxyllic acid to synthesize our LNPS, but I am using a DSPE-PEG(2000)-maleimide substitution that allows for peptide conjugation. I am testing this by synthesizing the DSPE-PEG(2000)-maleimide LNPs, testing their stability, and performing internalization assays with neutrophils. I am also testing a new formulation of PNPS using a maleimide-based linker. So far in this process, I have found that the DSPE-PEG(2000)-maleimide substitution in the LNPs does not affect its stability. I hypothesize that the DSPE-PEG(2000)-maleimide LNPs conjugated with peptide will be able to increase neutrophil internalization through surface nanomaterial interactions.