Choudhry M A, Messingham K A, Namak S, Colantoni A, Fontanilla C V, Duffner L A, Sayeed M M, Kovacs E J
Burn and Shock Trauma Institute, Loyola University Chicago Medical Center, 2160 South First Avenue, 60153, Maywood, IL, USA.
Alcohol. 2000 Jul;21(3):239-43. doi: 10.1016/s0741-8329(00)00093-8.
To understand the mechanism of suppressed immunity following alcohol consumption and thermal injury, we analyzed T cell functions in a mouse model of acute alcohol exposure and burn injury. Mice with blood alcohol levels at approximately 100 mg/dl were given a 15% scald or sham injury. Mice were sacrificed 48 h after injury. Our data demonstrated a 20-25% decrease in Con A-mediated splenic T cell proliferation (p<0.01) and 45-50% decrease in interleukin-2 (IL-2) production (p<0.01) following burn injury compared to the T cells from sham animals. A further decrease in the proliferation (25-30%) and IL-2 production (40-45%) was detected in T cells derived from burned animals receiving alcohol as compared to burn alone. No significant change in the proliferation and IL-2 production was observed in splenic T cells derived from sham-injured mice regardless of alcohol exposure. Additionally, there was no demonstrable difference in splenocyte apoptosis in any treatment group. These results suggest that alcohol consumption prior to burn injury causes a greater decrease in T cell proliferation and IL-2 production compared to either burn or alcohol injury alone that may further attenuate the cell-mediated immunity and thus enhance susceptibility to infection.
为了解饮酒和热损伤后免疫抑制的机制，我们在急性酒精暴露和烧伤的小鼠模型中分析了T细胞功能。将血液酒精水平约为100mg/dl的小鼠给予15%的烫伤或假损伤。损伤后48小时处死小鼠。我们的数据显示，与假手术动物的T细胞相比，烧伤后伴刀豆蛋白A（Con A）介导的脾T细胞增殖减少20%-25%（p<0.01），白细胞介素-2（IL-2）产生减少45%-50%（p<0.01）。与单纯烧伤相比，接受酒精的烧伤动物来源的T细胞增殖（25%-30%）和IL-2产生进一步减少（40%-45%）。无论是否暴露于酒精，假损伤小鼠来源的脾T细胞增殖和IL-2产生均未观察到显著变化。此外，任何治疗组的脾细胞凋亡均无明显差异。这些结果表明，与单独烧伤或酒精损伤相比，烧伤前饮酒导致T细胞增殖和IL-2产生的下降更大，这可能会进一步削弱细胞介导的免疫，从而增加感染易感性。
