STRESS AXIS, IMMUNE SYSTEM-DERIVED CYTOKINES AND ETHANOL

乙醇（Et）的消耗改变了生物燃料的某些监管方面。 下丘脑-垂体-肾上腺轴（HPAA）。 因为， 这个系统依赖于协调的合成和分泌 下丘脑的特定调节物质（例如，促肾上腺皮质激素 释放激素（CRH）;加压素（AVP）;生物胺），垂体- 压盖（例如，β内啡肽（BE）; ACTH）和肾上腺（例如， 儿茶酚胺;糖皮质激素）水平，我们一直在评估 Et在HPAA的每个水平上的影响。 激活HPAA或 皮质醇增多症伴随着短期和长期的Et消费 和Et戒断综合征 酗酒者通常会表现出一种伪- 库欣综合征，其中约17- 40%的酗酒者不 在第一周内对地塞米松抑制试验有反应 禁欲 由于糖皮质激素的相对升高状态（慢性 连续或慢性间歇性）可导致神经变化，甚至 细胞死亡，特别是在海马体中， 许多酗酒者的认知能力确实可能部分归因于 高皮质醇血症和随后的不可逆神经损伤 海马体和中枢神经系统的其他区域。 此外，委员会认为， 与双向通信的概念武装之间的 HPAA和免疫系统，我们正在探索是否确定 免疫系统衍生的细胞因子可以改善或加速 通过内分泌或旁分泌作用的神经死亡。 当然细胞因子 刺激不同类型的细胞以修复细胞损伤 通过细胞内信号放大， Et和糖皮质激素过度刺激选定的神经群体， 走向灭亡

Consumption of ethanol (Et) alters certain regulatory aspects of the hypothalamic-pituitary-adrenal axis (HPAA). Because the integrity of this system depends on the coordinated synthesis and secretion of specific regulatory substances at the hypothalamic (e.g., corticotropin- releasing hormone (CRH); vasopressin (AVP); biogenic amines), pituitary- gland (e.g., beta endorphin (BE); ACTH) and adrenal gland (e.g., catecholamines; glucocorticoids) level, we have been evaluating the impact of Et at each level of the HPAA. Activation of the HPAA or hypercortisolism accompanies both short- and long-term consumption of Et and the Et withdrawal syndrome. Alcoholics often present with a pseudo- Cushing's syndrome in which some 17-40 percent of alcoholics do not respond to the dexamethasone suppression test during the first week of abstinence. Since a relative state of elevated glucocorticoids (chronic continuous or chronic intermittent) can lead to neural changes and even cell death, particularly in the hippocampus, the progressive loss of cognitive capacity in many alcoholics may indeed be due in part to hypercortisolemia and subsequent irreversible neural damage in the hippocampus and other areas of the central nervous system. Furthermore, armed with the concept of the bidirectional communication between the HPAA and the immune system, we are exploring whether or not certain immune system-derived cytokines may be ameliorating or accelerating neural death through endocrine or paracrine actions. Certainly cytokines stimulate diverse cell types in an attempt to repair cellular damage through intracellular signal amplification which could in concert with Et and glucocorticoids overstimulate selected neural populations leading to their demise.