Wang Y, Huang D S, Giger P T, Watson R R
Department of Family and Community Medicine, University of Arizona, Tucson 85724.
Alcohol Clin Exp Res. 1994 Feb;18(1):64-70. doi: 10.1111/j.1530-0277.1994.tb00882.x.
Prolonged consumption of ethanol (ETOH) results in alterations of host defense via immune modulation, increasing susceptibility to infection. In the present study, effects of chronic dietary ETOH on cytokine production by splenocytes and thymocytes, splenocyte and thymocyte proliferation induced by mitogens, splenic natural killer cell activity, and antibody production (IgA and IgG) were examined. C57BL/6 mice were fed 5% ETOH v/v in the Lieber-DeCarli liquid diet for 11 weeks. Release of interleukin (IL)-2, IL-5, IL-6, IL-10, and interferon (IFN)-gamma produced by concanavalin A (Con A) stimulated splenocytes was significantly decreased, whereas secretion of IL-4 was slightly decreased by chronic dietary ETOH compared with controls. Production of tumor necrosis factor-alpha and IL-6 by lipopolysaccharide-stimulated splenocytes was significantly and slightly decreased by ETOH compared with controls, respectively. Splenocyte and thymocyte proliferation induced by Con A was significantly inhibited by ETOH, whereas splenocyte proliferation induced by lipopolysaccharide was not affected. Natural killer cell activity was significantly inhibited by ETOH compared with controls. The production of IgA and IgG by splenocytes were also significantly decreased by ETOH compared with controls. The levels of IL-2, IL-4, and IL-6 produced by Con A-stimulated thymocytes were significantly reduced by dietary ETOH compared with control, whereas production of IFN-gamma by thymocytes was not affected. Our results suggest that chronic dietary ETOH alters the cytokine release, thereby impairing immune response and T-cell maturation, which increase host susceptibility to infection.
长期摄入乙醇（ETOH）会通过免疫调节导致宿主防御功能改变，增加感染易感性。在本研究中，检测了慢性饮食ETOH对脾细胞和胸腺细胞细胞因子产生、丝裂原诱导的脾细胞和胸腺细胞增殖、脾自然杀伤细胞活性以及抗体产生（IgA和IgG）的影响。将C57BL/6小鼠在Lieber-DeCarli液体饮食中喂食5%（v/v）的ETOH，持续11周。与对照组相比，伴刀豆球蛋白A（Con A）刺激的脾细胞产生的白细胞介素（IL）-2、IL-5、IL-6、IL-10和干扰素（IFN）-γ的释放显著降低，而慢性饮食ETOH使IL-4的分泌略有降低。与对照组相比，ETOH分别使脂多糖刺激的脾细胞产生的肿瘤坏死因子-α和IL-6显著和略有降低。ETOH显著抑制了Con A诱导的脾细胞和胸腺细胞增殖，而脂多糖诱导的脾细胞增殖不受影响。与对照组相比，ETOH显著抑制了自然杀伤细胞活性。与对照组相比，ETOH也显著降低了脾细胞产生的IgA和IgG。与对照组相比，饮食ETOH使Con A刺激的胸腺细胞产生的IL-2、IL-4和IL-6水平显著降低，而胸腺细胞产生的IFN-γ不受影响。我们的结果表明，慢性饮食ETOH会改变细胞因子释放，从而损害免疫反应和T细胞成熟，增加宿主对感染的易感性。
