Neupane Sudan Prasad
Norwegian National Advisory Unit on Concurrent Substance Abuse and Mental Health Disorders, Innlandet Hospital Trust, Brumunddal, Norway; Norwegian Centre for Addiction Research (SERAF), University of Oslo, Oslo, Norway.
Front Immunol. 2016 Dec 27;7:655. doi: 10.3389/fimmu.2016.00655. eCollection 2016.
Bidirectional communication links operate between the brain and the body. Afferent immune-to-brain signals are capable of inducing changes in mood and behavior. Chronic heavy alcohol drinking, typical of alcohol use disorder (AUD), is one such factor that provokes an immune response in the periphery that, by means of circulatory cytokines and other neuroimmune mediators, ultimately causes alterations in the brain function. Alcohol can also directly impact the immune functions of microglia, the resident immune cells of the central nervous system (CNS). Several lines of research have established the contribution of specific inflammatory mediators in the development and progression of depressive illness. Much of the available evidence in this field stems from cross-sectional data on the immune interactions between isolated AUD and major depression (MD). Given their heterogeneity as disease entities with overlapping symptoms and shared neuroimmune correlates, it is no surprise that systemic and CNS inflammation could be a critical determinant of the frequent comorbidity between AUD and MD. This review presents a summary and analysis of the extant literature on neuroimmune interface in the AUD-MD comorbidity.
大脑与身体之间存在双向通信链路。传入的免疫至脑信号能够引起情绪和行为的变化。慢性重度饮酒是酒精使用障碍（AUD）的典型特征，是引发外周免疫反应的一个因素，该反应通过循环细胞因子和其他神经免疫介质最终导致脑功能改变。酒精还可直接影响小胶质细胞（中枢神经系统（CNS）的常驻免疫细胞）的免疫功能。多项研究表明特定炎症介质在抑郁症的发生和发展中起作用。该领域的现有证据大多来自关于孤立的AUD与重度抑郁症（MD）之间免疫相互作用的横断面数据。鉴于它们作为具有重叠症状和共享神经免疫相关性的疾病实体的异质性，系统性和中枢神经系统炎症可能是AUD与MD之间频繁共病的关键决定因素也就不足为奇了。本综述对AUD-MD共病中神经免疫界面的现有文献进行了总结和分析。
