Faunce D E, Gregory M S, Kovacs E J
Department of Cell Biology, Neurobiology, and Anatomy, The Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, Illinois 60153, USA.
J Leukoc Biol. 1997 Dec;62(6):733-40. doi: 10.1002/jlb.62.6.733.
To test the effects of acute ethanol exposure on immune function after thermal injury, mice with blood alcohol levels of 100 mg/dL were given a 15% total body surface area dorsal scald or sham injury. Bacterial challenge resulted in 100 and 40% mortality in burn + ethanol- and burn + vehicle-treated mice, respectively. Delayed-type hypersensitivity responses were also significantly suppressed in burn + ethanol-treated mice. At 1 and 4 days post-burn, concanavalin A (ConA) -induced total splenocyte proliferation in burn + ethanol-treated groups was significantly decreased (P < 0.01) compared with burn + vehicle- or sham-treated animals. This decrease was not observed in total splenocytes cultured with anti-CD3epsilon or among adherence-depleted splenocytes given ConA or anti-CD3epsilon. FACS analyses revealed no changes in splenocyte sub-type ratios in burn + ethanol mice. The data herein demonstrate that acute ethanol exposure before thermal injury results in enhanced susceptibility to bacterial infection and markedly suppressed cellular immunity, which appears to be macrophage dependent.
为了测试热损伤后急性乙醇暴露对免疫功能的影响，对血液酒精水平为100mg/dL的小鼠进行了15%体表面积的背部烫伤或假损伤。细菌攻击导致烧伤+乙醇处理组和烧伤+赋形剂处理组小鼠的死亡率分别为100%和40%。烧伤+乙醇处理组小鼠的迟发型超敏反应也受到显著抑制。在烧伤后1天和4天，与烧伤+赋形剂处理组或假处理组动物相比，烧伤+乙醇处理组中伴刀豆球蛋白A（ConA）诱导的总脾细胞增殖显著降低（P<0.01）。在用抗CD3ε培养的总脾细胞中或在给予ConA或抗CD3ε的去除黏附细胞的脾细胞中未观察到这种降低。流式细胞术分析显示烧伤+乙醇处理组小鼠脾细胞亚群比例没有变化。本文数据表明，热损伤前急性乙醇暴露会导致对细菌感染的易感性增加以及细胞免疫明显受到抑制，这似乎依赖于巨噬细胞。
