Alterations in Interleukin-2 Utilization by T-Cells from Rats Treated with an Ethanol-Containing Diet

Abstract

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.