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IRB No. 25-018-2 (Dr. Sheila Alessi, PI): Healthy Volunteer Registry (HVR)

The Healthy Volunteer Registry (HVR), is a program that the Clinical Research Center is starting to help support studies and other activities needing healthy volunteers. Individuals will voluntarily sign-up by self-reporting healthy and providing name, contact information and demographics through a REDCap link or QR code; or in-person/phone/email contact in the CRC. The HVR database will be used to support recruitment for CRC supported protocols and "other activities". The HVR data managers will maintain the database and share enrolled participants information according to the CRC supported study recruitment methods.

IRB No. 26-121-1 (Dr. Daniel Rosenberg, PI): Characterization of Cytokine Profiles and Urolithin A-Mediated Immune Modulation in PBMCs from Healthy Volunteers

This study aims to investigate how urolithin A, a compound produced when gut bacteria metabolize ellagitannins (naturally occurring plant polyphenols found in foods such as walnuts, pomegranates, and berries), modulates immune cytokine production in human peripheral blood mononuclear cells (PBMCs). Findings from our prior NIH-funded walnut supplementation study (UConn Health IRB #21-167JS-1) demonstrated decreased circulating pro-inflammatory cytokines (IL-21, IL-17A, GM-CSF) following walnut consumption. While these results suggest that walnut intake and urolithin A production reduce inflammatory signaling in vivo, the underlying cellular and molecular mechanisms remain unclear. To address this knowledge gap, we will enroll 3-10 healthy adult volunteers and collect a single fasting blood sample from each participant. PBMCs will be isolated and stimulated in vitro under different conditions: unstimulated, PMA/ionomycin-stimulated, and PMA/ionomycin with urolithin A exposure. Cytokine production will be quantified by ELISA, and flow cytometry will be used to identify immune cell subsets (CD4 , CD8 , etc.) responsible for cytokine secretion. This study will be conducted independently of our NIH-funded work and will not recontact or re-enroll prior participants. The results will establish baseline PBMC cytokine responses in individuals naïve to walnut supplementation, providing a control comparison for prior findings. Additionally, exploratory analyses will compare these results to de-identified data from previously identified high urolithin A producers to assess variability in cytokine modulation. Ultimately, this research will clarify how urolithin A influences inflammatory pathways in human immune cells, providing critical mechanistic insight into the immunomodulatory effects of dietary walnut-derived metabolites.

IRB No. 26-250J-1 (Dr. Santhanam Lakshminarayanan, PI): Understanding Glucose Metabolism in the Development and Treatment of Lupus

What Are We Studying? This study aims to better understand the changes that occur in the blood of people with and without lupus, and how different lupus treatments may influence these changes. You do not need to have lupus to be eligible to participate in this study. This may help identify new therapy targets that may reverse lupus. No study drugs will be given to any participants in this study. What Does Participation Involve? Participants enrolled in the study will be scheduled for a single one-hour study visit at UConn Health, Farmington, CT to answer questions about medical history and medications along with having a blood sample collected. Will I be Compensated? All study procedures performed will be at no charge and you will receive a $50 gift card to compensate for your participation.

IRB No. 26-130-2 (Dr. Beiyan Zhou, PI): Type 2 diabetes impact on dysregulated immune cell function in cardiovascular diseases

Type 2 diabetes (T2DM) is the leading cause of many serious health complications, including cardiovascular diseases, chronic kidney diseases, blindness, and several types of cancers. One of the primary disease-causing factors is malfunction of the immune system, which can lead to weakened immune cell function in fighting infections and sustained low-grade systemic chronic inflammation. Through direct and indirect effects, T2DM dysregulated immune cells are pathogenic factors in various disease conditions, including atherosclerosis, infection, autoimmune diseases, and cancerous transformation. T2DM is a primary cause for the marked increase of atherosclerotic cardiovascular disease (ASCVD), accounting for 30% of symptomatic cases. Accordingly, the ASCVD risk in T2DM patients is 2-4 fold more than that in the non-T2DM population. The concomitant increase of T2DM and ASCVD in the US has prompted the urgency for more accurate ASCVD risk assessment and an effective mitigation strategy direction. Current standard-of-care therapies, addressing factors such as lipid/hypertension/glycemic control, have underachieved as indicated by recent clinical trials and extensive cohort studies. Even novel drug classes approved for ASCVD prevention in T2DM, such as SGLT2 inhibitors or GLP-1 receptor agonists, reduce disease risk by only 2%. These results warrant a new direction in the mitigation strategy, which relies on advancing our understanding of immune cell function in T2DM and T2DM-associated ASCVD. Given the volatile and central roles of monocytes in ASCVD development and progression, we recently developed a set of new algorithms to annotate their function under complex conditions with high resolution. Importantly, powered by these tools, two distinct macrophage-derived foam cell development programs were revealed (homeostatic vs. pathogenic foaming). However, mechanisms underlying T2DM-altered monocyte-derived macrophage function in ASCVD pathogenesis remain elusive. This project aims to investigate cellular and molecular mechanisms derailed by T2DM in circulating immune cells; thus, samples from healthy or T2DM patients with or without cardiovascular diseases will be needed for this study. After completing this study, we may identify new molecular targets or develop comprehensive treatments for T2DM patients to reduce their risk of comorbidities, including ASCVD.