Ethanol-induced suppression of interleukin 1-like activity: reversal by a quinone derivative.

Chronic ethanol intake impairs several parameters of immune function. Since there is evidence that cytokine production by immune cells may contribute to the immunosuppressive effect of ethanol, we examined interleukin 1 (IL1) production by liver non-parenchymal cells (NPC) in ethanol-fed rats. Male Wistar rats (225-250 g) were fed by continuous intragastric infusion. The source of fat was either saturated fat or polyunsaturated fat. In addition, the effect of a quinone compound on IL1 production was assessed. Animals were fed for various periods: 1 week, 2 weeks, 1 month and 2 months. NPC were isolated and stimulated by lipopolysaccharide. IL1 production by NPC and the ratio of stimulated to unstimulated (S:U) IL1 production were evaluated in the different groups and related to the presence of liver injury. As expected, animals fed corn oil and ethanol (CO+E) developed pathologic liver injury, whereas animals fed saturated fat and ethanol (SF+E) had no liver injury. A progressive decrease in the S:U IL1 ratio was seen in the CO+E group over the 8-week period. The ratio in the SF+E group was higher. The quinone compound reversed the suppressive effect of ethanol on IL1 production. In summary, ethanol-induced suppression of IL1 production was modulated by diet and the presence of liver injury. This suppression of IL1 production was reversed by a quinone compound; the exact mechanism for the reversal of this inhibition is unknown.