Ethanol-induced alterations in lymphocyte function in the guinea pig

• Published in: Alcoholism, clinical and experimental research Vol. 8; no. 1; p. 62
• Main Authors: Roselle, G A, Mendenhall, C L
• Format: Journal Article
• Language: English
• Published: England 01.01.1984
• Subjects: Animals; Ethanol - pharmacology; Guinea Pigs; Leukocyte Count; Lymphocyte Activation - drug effects; Lymphocytes - drug effects; Lymphocytes - physiology; Macrophage Migration-Inhibitory Factors; Skin Tests
• ISSN: 0145-6008

Infections and chronic liver injury are common causes of morbidity and mortality in alcoholics, and both of these may be related to an altered immune response. This study describes a guinea pig model of chronic ethanolism designed to selectively study the cellular immune system in a setting free from the malnutrition, socioeconomic deprivation, and severe underlying hepatic dysfunction seen in human disease. Animals were given 2.5 g/kg/day of ethanol as a 15% solution in 0.9% NaCl or isocaloric-dextrose-saline control solution intraperitoneally in 2 divided doses for 5 weeks. At 2 weeks, the mean serum ethanol level 1 hr after treatment was 20.4 mM (range 8.9-30.6) while the mean serum acetaldehyde level was 55.1 microM (range 17.0-111). At 5 weeks the serum levels for ethanol and acetaldehyde were 20.1 mM (13.3-32.9) and 41.5 microM (2.4-87.6), respectively. Weight gain was persistent throughout the study and did not differ significantly between ethanol and control groups. After 5 weeks of treatment, lymphocyte response to the mitogens, phytohemagglutinin, and concanavalin A was significantly decreased in the ethanol treated group (p less than 0.05). Response to the specific antigen, picrylated human serum albumin, T & B cell per cent and number, skin test reactivity, peripheral white blood cell count, total lymphocyte count, and migration inhibitory factor production were not significantly altered by 5 weeks of ethanol treatment. Therefore, in a controlled animal model of chronic ethanolism, we observed a significant depression of lymphocyte blastogenic response which may, in part, explain the increased propensity to infection by intracellular pathogens seen in alcoholics.