Ethanol-induced alterations in lymphocyte function in the guinea pig

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.