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）。 因为这件事的完整性 系统依赖于特定的协调合成和分泌 下丘脑的调节物质[（例如，激素释放 激素（CRH）;加压素（AVP）;生物胺）]，垂体腺 [（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，我们一直在评估影响 在每个层次的HPAA。 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%的酗酒者对酒精无反应。 在禁欲的第一周进行地塞米松抑制试验。 由于糖皮质激素升高的相对状态（慢性持续性或 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，认知功能的逐渐丧失 许多酗酒者的饮酒能力确实可能部分是由于高皮质醇血症 以及随后在海马体和其他部位造成的不可逆的神经损伤 中枢神经系统的区域。 此外，有了这个概念， HPAA和免疫系统之间的双向交流。 我们正在探索是否某些免疫系统衍生的细胞因子 可能是通过内分泌或 旁分泌作用 当然，细胞因子刺激不同类型的细胞， 试图通过细胞内信号修复细胞损伤 扩增可能与Et和糖皮质激素有关 过度刺激特定的神经细胞群导致其死亡

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% 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.