ALTERATIONS IN INTERLEUKIN-2 UTILIZATION BY T-CELLS FROM RATS TREATED WITH AN ETHANOL-CONTAINING DIET

Administration of ethanol to Sprague‐Dawley rats has been shown to produce a defect in lymphocyte proliferation in response to concanavalin A. Because a critical element in T‐cell proliferation is the production of interleukin‐2, experiments were designed to evaluate the influence of ethanol on the production and utilization of interleukin‐2 by spleen cells from ethanol‐treated animals. To ensure that changes in spleen cell responses to mitogenic stimulation were not simply caused by a loss of responding T cells, we tested nylon wool‐nonadherent cells. The response to concanavalin A of isolated T cells from ethanol‐treated rats was consistently less than that of equivalent numbers of cells from control animals. The addition of recombinant interleukin‐2 to cultures of T cells did not correct the defect in proliferation to concanavalin A noted in cells from ethanol‐treated rats. Further study results demonstrated that interleukin‐2 production by T cells from ethanol‐treated animals was equal to or greater than that by cells from animals given control diet. Blast cells recovered from 48‐hr concanavalin A‐stimulated spleen cell cultures from ethanol‐treated animals, however, showed a decreased ability to proliferate in response to exogenous interleukin‐2. Binding of 125I‐interleukin‐2 to blast cells resulting from concanavalin A stimulation, under conditions that detected high‐affinity binding, was similar in cells from treated and control animals. These data indicate that the deficiency in proliferation of lymphocytes from ethanol‐treated animals is not caused by a lack of interleukin‐2 production by the T cells. It is also apparent that T cells from ethanol‐treated rats are not deficient in high‐affinity interleukin‐2 receptors. Copyright © 1990, Wiley Blackwell. All rights reserved