Ethanol-induced modulation of cytokine production by splenocytes during murine retrovirus infection causing murine AIDS.
Ethanol-induced modulation of cytokine production by splenocytes during murine retrovirus infection causing murine AIDS.
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在导致小鼠艾滋病的小鼠逆转录病毒感染过程中，乙醇诱导调节脾细胞产生的细胞因子。
DOI：
10.1111/j.1530-0277.1993.tb05660.x
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Watson,RR
中科院分区：
文献类型：
--
作者：
Wang,Y;Huang,DS;Giger,PT;Watson,RR
乙醇（ETOH）的消耗与免疫反应的一般抑制有关，导致对感染的易感性增加。慢性饮食ETOH消耗可能是逆转录病毒感染后加速人类获得性免疫缺陷综合征（AIDS）发展的辅助因素之一。对接种导致小鼠AIDS的LP-BM 5逆转录病毒的雌性C57 BL/6小鼠饲喂Lieber-DeCarli液体饲料中的慢性饮食ETOH [5%（v/v）] 11周。由于细胞因子是体液和细胞免疫的关键调节因子，因此通过ELISA方法测量伴刀豆球蛋白A（ConA）和脂多糖（LPS）诱导的脾细胞产生的细胞因子。逆转录病毒感染引起的白细胞介素（IL）-2水平降低保持不变。逆转录病毒感染期间ConA刺激的脾细胞在体外产生的IL-5和IL-6水平升高，饮食ETOH显著进一步增加。逆转录病毒感染导致的IL-4升高不受饮食ETOH的影响。然而，由逆转录病毒感染诱导的IL-10的产生增加被饮食ETOH显著降低，而由逆转录病毒感染诱导的干扰素-r的释放减少被显著增强。饮食ETOH可显著进一步增加逆转录病毒感染小鼠经LPS刺激的脾细胞产生的升高水平的肿瘤坏死因子-a，而LPS刺激的脾细胞产生的IL-6水平不受影响。由逆转录病毒感染引起的抑制T细胞增殖被饮食ETOH进一步显著降低。然而，未观察到饮食ETOH对逆转录病毒感染引起的B-细胞增殖降低的影响。这些结果表明，饮食ETOH加速了导致艾滋病的免疫功能障碍的进展，因为饮食ETOH改变了免疫调节细胞因子的产生。
Ethanoi (ETOH) consumption has been associated with general suppression of the immune response, resulting in increased susceptibility to infection. Chronic dietary ETOH consumption may be one of the cofactors accelerating development of human acquired immune deficiency syndrome (AIDS) after retrovirus infection. Chronic dietary ETOH [5% (v/v)] in the Lieber‐DeCarli liquid diet was fed female C57BL/6 mice inoculated with LP‐BM5 retrovirus causing murine AIDS for 11 weeks. Because cytokines are key regulators of humoral and cellular immunity, their production by concanavalin A (ConA) and lipopolysaccharide (LPS)‐induced splenocytes was measured by ELISA methods. Decreased levels of interleukin (IL)‐2 caused by retrovirus infection remained unchanged. Elevated levels of IL‐5 and IL‐6 produced in vitro by ConA‐stimulated spleen cells during retrovirus infection were significantly further increased by dietary ETOH. Elevated IL‐4 due to retroviral infection were not affected by dietary ETOH. Increased production of IL‐10 induced by retrovirus infection, however, was significantly reduced by dietary ETOH, whereas decreased release of interferon‐r induced by retrovirus infection was significantly enhanced. Elevated levels of tumor necrosis factor‐a produced by LPS‐stimulated splenocytes from retrovirus infected mice were significantly further increased by dietary ETOH, whereas levels of IL‐6 by LPS‐stimulated splenocytes were not affected. Suppressed T‐cell proliferation caused by retrovirus infection was significantly reduced further by dietary ETOH. However, no effect of dietary ETOH was observed on decreased B‐cell proliferation by retrovirus infection. These results suggest that dietary ETOH aggravates progression of immune dysfunction leading to AIDS, because dietary ETOH modifies production of immunological regulatory cytokines.