Regulation of Liver Inflammation and Infection by Albumin Following Alcohol Exposure
Abstract
Alcohol-associated liver disease (ALD), a consequence of chronic ethanol consumption, is an increasing health concern characterized by immune dysfunction and enhanced susceptibility to infection. Albumin, the most abundant circulating protein synthesized in the liver, is significantly decreased in individuals who excessively consume alcohol. Previous studies have shown that albumin has an important role in regulating immune cell activity following ethanol feeding, potentially impacting the response to bacterial pathogens. However, how albumin regulates ethanol-induced immune cell composition in the liver after ethanol feeding and how this could affect the liver’s response to bacterial infection remains unclear. This study aims to determine how these factors regulate immune cell recruitment and the liver’s response to Klebsiella Pneumoniae (K.P.) infection. We hypothesize that lower albumin levels will result in decreased recruitment of inflammatory immune cells to the liver, consequently reducing the inflammatory burden and necrotic liver damage. To test this hypothesis, ethanol-fed mice with varying albumin concentrations are examined using histology and immunohistochemistry analyses to characterize immune cell populations in liver tissue. Following K.P. infection, liver necrosis is quantified to assess the extent of liver damage caused by inflammation. Based on previous data, mice with lower albumin levels are expected to exhibit reduced inflammatory cell accumulation and decreased liver necrosis, compared with control groups. Overall, this research provides insight into albumin’s contribution to immune responses during alcohol exposure and its influence on susceptibility to bacterial infection.
Start Time
15-4-2026 9:00 AM
End Time
15-4-2026 12:00 PM
Room Number
Culp Ballroom 316
Poster Number
68
Presentation Type
Poster
Student Type
Undergraduate Student
Faculty Mentor
Bryan Mackowiak
Regulation of Liver Inflammation and Infection by Albumin Following Alcohol Exposure
Culp Ballroom 316
Alcohol-associated liver disease (ALD), a consequence of chronic ethanol consumption, is an increasing health concern characterized by immune dysfunction and enhanced susceptibility to infection. Albumin, the most abundant circulating protein synthesized in the liver, is significantly decreased in individuals who excessively consume alcohol. Previous studies have shown that albumin has an important role in regulating immune cell activity following ethanol feeding, potentially impacting the response to bacterial pathogens. However, how albumin regulates ethanol-induced immune cell composition in the liver after ethanol feeding and how this could affect the liver’s response to bacterial infection remains unclear. This study aims to determine how these factors regulate immune cell recruitment and the liver’s response to Klebsiella Pneumoniae (K.P.) infection. We hypothesize that lower albumin levels will result in decreased recruitment of inflammatory immune cells to the liver, consequently reducing the inflammatory burden and necrotic liver damage. To test this hypothesis, ethanol-fed mice with varying albumin concentrations are examined using histology and immunohistochemistry analyses to characterize immune cell populations in liver tissue. Following K.P. infection, liver necrosis is quantified to assess the extent of liver damage caused by inflammation. Based on previous data, mice with lower albumin levels are expected to exhibit reduced inflammatory cell accumulation and decreased liver necrosis, compared with control groups. Overall, this research provides insight into albumin’s contribution to immune responses during alcohol exposure and its influence on susceptibility to bacterial infection.
