DIETARY VITAMIN-E MODULATION OF CYTOKINE PRODUCTION BY SPLENOCYTES AND THYMOCYTES FROM ALCOHOL-FED MICE

As vitamin E enhances immune responses, it may reduce dietary ethanol (EtOH) induced immune suppression, thereby favorably affecting host di sease resistance. The effects of dietary vitamin E at higher level in alcohol-fed female C57BL/6 mice was determined via in vitro cytokine p roduction by splenocytes and thymocytes, and some other immune functio ns. A 15-fold increase of vitamin E (160 IU/liter) in a liquid diet (N ational Council Research), with or without EtOH (4.5%, v/v), was fed t o mice for 10 weeks. Vitamin E supplementation restored production of interleukin-2, -5, -6, -10, and interferon-gamma by concanavalin A (Co n A)-stimulated splenocytes and interleukin-6 and tumor necrosis facto r-alpha by lipopolysaccharide-stimulated splenocytes, which were suppr essed by dietary EtOH. However, it had no effect on interleukin-4 secr etion, which was also reduced by splenocytes from EtOH-fed mice. Vitam in E supplementation also restored EtOH-suppressed, mitogen induced sp lenocyte proliferation, but not thymocyte proliferation, although it s lightly increased production of immunoglobulin A and G by lipopolysacc haride-stimulated splenocytes, which were suppressed by dietary EtOH. Dietary vitamin E, furthermore, significantly increased interleukin-2 and -6 secretion by Con A-stimulated thymocytes, which were suppressed by dietary EtOH, although it had no effect on interleukin-4 and inter feron-gamma production by Con A-stimulated thymocytes from EtOH-fed mi ce. These data suggest that dietary vitamin E supplementation can modu late dysregulation of cytokines initiated by dietary EtOH and restore immune dysfunctions induced by EtOH ingestion.