TY - JOUR
T1 - Dietary Vitamin E Modulation of Cytokine Production by Splenocytes and Thymocytes from Alcohol‐Fed Mice
AU - Wang, Yuejian
AU - Huang, Dennis S.
AU - Watson, Ronald R.
PY - 1994/4
Y1 - 1994/4
N2 - As vitamin E enhances immune responses, it may reduce dietary ethanol (EtOH)‐induced immune suppression, thereby favorably afffecting host disease resistance. The effects of dietary vitamin E at higher level in alcohol‐fed female C57BL/6 mice was determined via in vitro cytokine production by splenocytes and thymocytes, and some other immune functions. A 15‐fold increase of vitamin E (160IU/liter) in a liquid diet (National Council Research), with or without EtOH (4.5%, v/v), was fed to mice for 10 weeks. Vitamin E supplementation restored production of interleukin‐2, ‐5, ‐6, ‐10, and inter‐feron‐γ by concanavalin A (Con A)‐stimulated splenocytes and in terleukin‐6 and tumor necrosis factor‐a by lipopolysaccharide‐stimulated splenocytes, which were suppressed by dietary EtOH. However, it had no effect on interleukin‐4 secretion, which was also reduced by splenocytes from EtOH‐fed mice. Vitamin E supplementation also restored EtOH‐suppressed, mitogen‐induced splenocyte proliferation, but not thymocyte proliferation, although it slightly increased production of immunoglobulin A and G by lipopolysaccha‐ride‐stimulated splenocytes, which were suppressed by dietary EtOH. Dietary vitamin E, furthermore, significantly increased interleu‐kin‐2 and ‐6 secretion by Con A‐stimulated thymocytes, which were suppressed by dietary EtOH, although it had no effect on interleukin‐ 4 and interferon‐γ production by Con A‐stimulated thymocytes from EtOH‐fed mice. These data suggest that dietary vitamin E supple‐mentation can modulate dysregulation of cytokines initiated by dietary EtOH and restore immune dysfunctions induced by EtOH ingestion.
AB - As vitamin E enhances immune responses, it may reduce dietary ethanol (EtOH)‐induced immune suppression, thereby favorably afffecting host disease resistance. The effects of dietary vitamin E at higher level in alcohol‐fed female C57BL/6 mice was determined via in vitro cytokine production by splenocytes and thymocytes, and some other immune functions. A 15‐fold increase of vitamin E (160IU/liter) in a liquid diet (National Council Research), with or without EtOH (4.5%, v/v), was fed to mice for 10 weeks. Vitamin E supplementation restored production of interleukin‐2, ‐5, ‐6, ‐10, and inter‐feron‐γ by concanavalin A (Con A)‐stimulated splenocytes and in terleukin‐6 and tumor necrosis factor‐a by lipopolysaccharide‐stimulated splenocytes, which were suppressed by dietary EtOH. However, it had no effect on interleukin‐4 secretion, which was also reduced by splenocytes from EtOH‐fed mice. Vitamin E supplementation also restored EtOH‐suppressed, mitogen‐induced splenocyte proliferation, but not thymocyte proliferation, although it slightly increased production of immunoglobulin A and G by lipopolysaccha‐ride‐stimulated splenocytes, which were suppressed by dietary EtOH. Dietary vitamin E, furthermore, significantly increased interleu‐kin‐2 and ‐6 secretion by Con A‐stimulated thymocytes, which were suppressed by dietary EtOH, although it had no effect on interleukin‐ 4 and interferon‐γ production by Con A‐stimulated thymocytes from EtOH‐fed mice. These data suggest that dietary vitamin E supple‐mentation can modulate dysregulation of cytokines initiated by dietary EtOH and restore immune dysfunctions induced by EtOH ingestion.
KW - Cytokines
KW - Ethanol
KW - Immunoglobulin
KW - T‐cell Maturation
KW - Vitamin E
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U2 - 10.1111/j.1530-0277.1994.tb00025.x
DO - 10.1111/j.1530-0277.1994.tb00025.x
M3 - Article
C2 - 8048738
AN - SCOPUS:0028355158
SN - 0145-6008
VL - 18
SP - 355
EP - 362
JO - Alcoholism: Clinical and Experimental Research
JF - Alcoholism: Clinical and Experimental Research
IS - 2
ER -