ETHANOL-CONSUMPTION SUPPRESSES THE IL2-INDUCED PROLIFERATION OF NK CELLS

Ethanol (20% w/v) given to female, C57BL/6 mice in their drinking wate r suppresses natural killer (NK) and lymphokine activated killer cell cytolytic activity in mixed splenocytes and in splenocytes highly enri ched for NK cells. The present study examined the effects of ethanol c onsumption on rIL2-induced proliferation of enriched NK cells. Mice we re given 20% w/v ethanol in the drinking water for 2 weeks. Splenic NK cells were harvested and enriched up to 88% based on surface expressi on of NK1.1. The enriched NK cells were cultured in the presence of 10 00 IU/ml (20 pg/ml) murine recombinant interleukin 2 (rIL2). There wer e fewer cells (p < 0.02) from ethanol-consuming mice compared to cells from water-drinking control mice after incubation with IL2 at 2, 4, a nd 6 days of culture. Ethanol consumption was associated with signific antly lower [H-3]thymidine uptake (p < 0.05). Ethanol consumption did not affect apoptosis or intracellular levels of interferon-gamma, tumo r necrosis factor-alpha, or granulocyte macrophage colony-stimulating factor in NK cells. Ethanol consumption did not affect the expression of c-myc mRNA in NK cells that were cultured for 10 min or 4, 8, and 1 8 hr in rIL2. Suppression of IL2-induced NK cell proliferation is asso ciated with ethanol consumption, and suppression is not due to altered IL2 receptor expression, increased apoptosis, intracellular cytokine levels, or c-myc expression. (C) 1996 Academic Press, Inc.