Albumin Regulates Ethanol-Induced Inflammatory Responses in T-Cells
Abstract
Heavy alcohol consumption has been shown to disrupt normal immune function and increase inflammation, but the mechanisms linking alcohol exposure to immune responses are not fully understood. Previous studies in both patients and mouse models have found that inflammatory pathways, particularly those involving T-cells, are associated with changes in circulating albumin levels after heavy alcohol use. These findings suggest that albumin may play an important role in regulating immune responses during alcohol exposure. The goal of this project is to determine how ethanol, its metabolite acetaldehyde, and albumin work together to influence inflammatory signaling in T-cells. We hypothesize that higher albumin levels will enhance T-cell immune activation, while lower albumin levels will reduce the inflammatory response, especially in the presence of ethanol. To test this hypothesis, Jurkat T-cells, an immortalized human T-cell line, are treated with combinations of ethanol, acetaldehyde, and albumin, followed by stimulation with inflammatory activators of T-Cell signaling. Changes in inflammatory and activation-related pathways will be measured using quantitative PCR to assess gene expression and western blotting to analyze protein levels. Based on prior data and ongoing cell culture experiments, we expect that albumin will significantly alter how T-cells respond to ethanol and acetaldehyde, with reduced albumin leading to a dampened inflammatory response. Overall, this project aims to better understand how alcohol-induced changes in albumin levels contribute to immune dysfunction, which may help explain altered inflammatory responses seen in individuals with heavy alcohol use.
Start Time
15-4-2026 1:30 PM
End Time
15-4-2026 4:30 PM
Room Number
Culp Ballroom 316
Poster Number
64
Presentation Type
Poster
Student Type
Undergraduate Student
Faculty Mentor
Bryan Mackowiak
Albumin Regulates Ethanol-Induced Inflammatory Responses in T-Cells
Culp Ballroom 316
Heavy alcohol consumption has been shown to disrupt normal immune function and increase inflammation, but the mechanisms linking alcohol exposure to immune responses are not fully understood. Previous studies in both patients and mouse models have found that inflammatory pathways, particularly those involving T-cells, are associated with changes in circulating albumin levels after heavy alcohol use. These findings suggest that albumin may play an important role in regulating immune responses during alcohol exposure. The goal of this project is to determine how ethanol, its metabolite acetaldehyde, and albumin work together to influence inflammatory signaling in T-cells. We hypothesize that higher albumin levels will enhance T-cell immune activation, while lower albumin levels will reduce the inflammatory response, especially in the presence of ethanol. To test this hypothesis, Jurkat T-cells, an immortalized human T-cell line, are treated with combinations of ethanol, acetaldehyde, and albumin, followed by stimulation with inflammatory activators of T-Cell signaling. Changes in inflammatory and activation-related pathways will be measured using quantitative PCR to assess gene expression and western blotting to analyze protein levels. Based on prior data and ongoing cell culture experiments, we expect that albumin will significantly alter how T-cells respond to ethanol and acetaldehyde, with reduced albumin leading to a dampened inflammatory response. Overall, this project aims to better understand how alcohol-induced changes in albumin levels contribute to immune dysfunction, which may help explain altered inflammatory responses seen in individuals with heavy alcohol use.
