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随着现代人们生活水平的提高、生活节奏的加快以及压力的增加,酒精的消费量与饮酒的人数在不断增加。近年来,随着免疫毒理学概念的提出及相关研究的不断深入,酒精的免疫毒性也越来越受到人们的关注,并得到了广泛研究。长期饮酒对机体免疫系统有抑制作用,已有文献报道酒精及其代谢产物可抑制淋巴细胞的活性,影响抗体生成,对T淋巴细胞的抑制作用尤为明显,并且对淋巴细胞的抑制作用呈剂量依赖性,此外对自然杀伤细胞也有抑制作用。妊娠期饮酒对新生儿免疫系统的损伤很大,可引起新生儿酒精综合征,不仅影响固有免疫,还能造成新生儿适应性免疫缺陷,使其更容易受到各种病菌感染。临床及动物实验均证实了妊娠期及哺乳期持续的酒精暴露可影响新生儿的免疫系统,甚至一直持续到成年。Karen等通过测定出生前后持续酒精暴露的小鼠的胸腺、脾脏等脏器中淋巴细胞数量及活性,发现酒精可能通过抑制胸腺中T淋巴细胞的成熟影响其活性,进而影响免疫反应。长期过量饮酒还易引起酒精性肝损伤(ALD),而ALD患者体内普遍存在体液免疫和细胞免疫的异常,使患者免疫力低下。乙醇在肝脏中分解为乙醛,而乙醛蛋白加合物可引起肝脏的炎症反应,进而引起免疫损伤。酒精还可引发肝脏脂质过氧化,产生丙二醛等过氧化产物,而丙二醛和乙醛又可以相互作用形成丙二醛乙醛加合物(MAA),可刺激机体产生大量抗MAA抗体,这些抗体与酒精性肝损伤的严重程度有关。另外,一些细胞因子如白细胞介素、肿瘤坏死因子等在酒精对肝脏的免疫毒性中发挥重要作用。长期酗酒者体内还可产生自身抗体,可促进肝细胞的功能损伤并破坏细胞。尽管长期或大量酒精暴露才能引起机体免疫系统的损伤,但有文献报道酒精与其他药物合用时可能会影响酒精的毒性作用。有研究表明,与单独给予酒精相比,对乙酰氨基酚与酒精联合应用可明显加剧酒精的免疫毒性。另有文献表明,联苯双酯与酒精联用时,可明显改善酒精引起的细胞免疫毒性作用。总之,酗酒对人体免疫系统有很大的损害,孕妇饮酒更能影响胎儿免疫系统的发育,使其出生后免疫反应受到抑制,甚至持续到成人时期。酒精与一些药物合用可能导致毒性的改变,值得关注。
With the improvement of modern people’s living standard, the accelerated pace of life and the increase of pressure, the number of consuming and drinking alcohol continues to increase. In recent years, with the introduction of the concept of immunotoxicology and the deepening of related research, the immunotoxicity of alcohol has drawn more and more attention and been extensively studied. Long-term drinking on the body’s immune system inhibition, it has been reported in the literature alcohol and its metabolites can inhibit lymphocyte activity, affecting antibody production, especially for T lymphocyte inhibition, and lymphocyte inhibition in a dose-dependent manner In addition, natural killer cells also have inhibitory effect. Gestational drinking is very damaging to the newborn’s immune system and can cause neonatal alcohol syndrome that affects not only innate immunity but also adaptive immunodeficiency in newborns making them more susceptible to various germs. Both clinical and animal experiments confirm that continued alcohol exposure during pregnancy and lactation can affect the newborn’s immune system and persist until adulthood. Karen et al. By measuring the number and activity of lymphocytes in the thymus, spleen and other organs of mice exposed to persistent alcohol exposure before and after birth, we found that alcohol may affect the immune response by inhibiting the maturation of T lymphocytes in the thymus. Long-term excessive drinking is also likely to cause alcoholic liver injury (ALD), while ALD patients generally exist in humoral and cellular immune abnormalities, so that patients with low immunity. Ethanol breaks down into acetaldehyde in the liver, whereas acetaldehyde adduct can cause inflammation in the liver, which in turn can cause immune damage. Alcohol can also lead to liver lipid peroxidation, produce malondialdehyde and other peroxidation products, and malondialdehyde and acetaldehyde can interact with the formation of malondialdehyde acetaldehyde adduct (MAA), can stimulate the body to produce a large number of anti-MAA Antibodies, these antibodies and the severity of alcoholic liver injury related. In addition, some cytokines such as interleukins and tumor necrosis factor play an important role in the immunotoxicity of alcohol to the liver. Long-term alcoholics can also produce autoantibodies in the body, can promote the functional damage of liver cells and damage cells. Although long-term or extensive alcohol exposure can cause damage to the body’s immune system, it has been reported in the literature that alcohol and other drugs may affect the toxic effects of alcohol. Studies have shown that, compared with alcohol alone, the combination of acetaminophen and alcohol can significantly aggravate the immunotoxicity of alcohol. Another literature shows that bifendate and alcohol when used, can significantly improve the alcohol-induced cellular immune toxicity. In short, alcoholism has great damage to the human immune system, pregnant women drinking more affect the development of fetal immune system, immune response after birth is inhibited, and even continued into adulthood. Alcohol and some drugs may lead to changes in toxicity, it is worth attention.