Influence of ethanol consumption on immune competence of adult animals exposed to ethanol in utero
Influence of ethanol consumption on immune competence of adult animals exposed to ethanol in utero
复制标题
DOI：
10.1111/j.1530-0277.1998.tb03665.x
复制
发表时间：
1998-04-01
影响因子：
3.2
通讯作者：
Weinberg, J
中科院分区：
文献类型：
--
作者：
Jerrells, TR;Weinberg, J
乙醇消耗导致实验动物和人类免疫系统的显著变化。我们和其他人以前的工作已经确定，在子宫内暴露于乙醇会导致后代免疫系统的改变，并持续到成年。本研究旨在确定产前暴露于乙醇是否会导致成年后乙醇摄入对免疫抑制作用的脆弱性增加。从产前乙醇组（E）、配对喂养组（PF）和自由喂养对照组（C）中选择成年雄性和雌性Sprague-Dawley后代，并给予含乙醇的液体饮食或配对喂养不含乙醇的等热量液体饮食30天。在30天喂养期结束时，淋巴细胞对有丝分裂原伴刀豆球蛋白A（Con A）和脂多糖的反应，和白细胞介素-2（IL-2）的活性。本研究的结果支持并扩展了先前的数据，这些数据证明了产前乙醇暴露对T细胞对有丝分裂原的反应的长期不利影响，并提供了进一步的证据，即男性后代的缺陷似乎比女性后代更稳健。与产前PF和C对应物相比，产前E男性显示出对Con A的T淋巴细胞增殖减少，对IL-2的T淋巴母细胞增殖减少，无论他们成年后是接触乙醇还是对照饮食。此外，T-淋巴母细胞增殖IL-2被抑制在产前E，与产前C相比，女性暴露于控制饮食在成年期。这是第一次报告的赤字在T细胞方面的免疫E女性，虽然它似乎，这种赤字可能已部分介导的营养作用。本研究的第二个主要发现是，成年期摄入乙醇饮食本身对男性和女性的T细胞反应具有显着的免疫抑制作用。然而，与我们的预期相反，先前在子宫内暴露于乙醇并没有加剧成年乙醇消耗后观察到的免疫反应性的变化。
Ethanol consumption results in significant changes in the immune system of experimental animals and humans. Previous work by ourselves and others has established that in utero exposure to ethanol results in alterations in the immune system of the offspring that persist into adult life. The present study was designed to determine if prenatal exposure to ethanol results in increased vulnerability to the immunosuppressive effects of ethanol consumption in adulthood. Male and female Sprague-Dawley offspring were selected in adulthood from prenatal ethanol (E), pair-fed (PF), and ad libitum-fed control (C) groups, and given either an ethanol-containing liquid diet or were pair-fed an isocaloric liquid diet without ethanol for 30 days, At the end of the 30-day feeding period, lymphocyte responses to the mitogens concanavalin A (Con A) and lipopolysaccharide, and to interleukin-2 (IL-2) were tested using in vitro assays. The results of this study support and extend previous data demonstrating longterm adverse effects of prenatal ethanol exposure on T-cell responses to mitogens, and provide further evidence that deficits seem to be more robust in male than in female offspring, Prenatal E males showed reduced T-lymphocyte proliferation to Con A and T-lymphoblast proliferation to IL-2, compared with their prenatal PF and C counterparts, regardless of whether they were exposed to the ethanol or the control diet in adulthood. In addition, T-lymphoblast proliferation to IL-2 was suppressed in prenatal E, compared with prenatal C, females exposed to control diet in adulthood. This is the first report of a deficit in T-cell aspects of immunity in E females, although it appears that this deficit may have been partially mediated by nutritional effects. A second major finding in this study is that consumption of ethanol diet in adulthood in itself had significant immunosuppressive effects on T-cell responses in both males and females. However, contrary to our expectation, previous exposure to ethanol in utero did not exacerbate the changes in immune responsiveness that were observed after adult ethanol consumption.