The influence of acute and chronic ethanol or bourbon administration on phagocytic and immune responses in rats

Abstract

The acute oral administration of ethanol or the alcoholic beverage, bourbon, to rats did not alter the intravascular clearance rate of 51Cr-labeled sheep red blood cells (SRBC). Hepatic localization of the 51Cr-SRBC in ethanol- and bourbon-treated rats was comparable, on a per weight basis, to that manifested by sucrose control animals. Similarly, pulmonary and splenic uptake of 51CR-SRBC in rats receiving ethanol or bourbon 24 hr prior to administration of the 51Cr-SRBC was unchanged from control values; however, in rats intubated with ethanol or bourbon 16 hr prior to 51Cr-SRBC injection, splenic uptake was significantly impaired. Pulmonary localization of the 51Cr-SRBC was reduced in rats intubated with bourbon 16 hr prior to the labeled erythrocyte administration; ethanol-treated rats manifested pulmonary uptake comparable to controls. In rats that were intubated with ethanol or bourbon 3.5 hr prior to 51Cr-SRBC, splenic localization of the radioactivity was unchanged from control values; however, ethanol-treated rats manifested a significantly greater pulmonary localization than control animals. Associated with the normal phagocytic activity in the acute ethanol- or bourbon-treated animals was a normal peak primary hemagglutinin response and a normal secondary immune response. However, in rats on a chronic diet containing ethanol or bourbon, in which ethyl alcohol contributed 50% of the total calories, a significantly reduced primary immune response was manifested. This impaired ability to mount a normal primary immune response was associated with a normal vascular clearance of the 51CR-SRBC and a normal secondary immune response. Predicated upon the hypothesis that the macrophage plays an integral role in the initiation of the immune response, it is suggested that acute alcohol ingestion does not impair macrophage function, as evidenced by the normal phagocytic activity and concomitant immune response, but chronic alcohol ingestion may impair either the presentation of the antigen by the macrophage to an antibody-producing cell or the interaction of the macrophage with other immunocompetent cells. Although the extrapolation of the experimental data in the present study to the chronic alcoholic is tenuous, it is suggested that macrophage dysfunction could contribute to the altered immunological responsiveness observed in the chronic alcoholic.