Citation

Neupane SP. Front. Immunol. 2016; 7: e655.

Affiliation

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.

Copyright

(Copyright © 2016, Frontiers Research Foundation)

DOI

10.3389/fimmu.2016.00655

PMID

28082989

Abstract

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.

Language: en

Keywords

alcohol drinking; alcohol use disorder; comorbidity; cytokines; depression; neuroimmune interface; neuroinflammation