Mechanisms of Stress-Dependent Neuroinflammation and Their Implications for Understanding Consequences of Alcohol Exposure

Abstract

There is a rich history of studies examining the impact of acute and chronic stress challenges—and the hormonal responses they evoke—on immunological function. Such studies generally fall within the realm of stress-induced immunomodulation and involve exposure of test subjects to various stress challenges in some combination with exposure to an antigen (e.g., lipopolysaccharide; LPS), a replicating pathogen (bacteria, viruses, etc.), or direct wound infliction. The net outcome in these types of studies is that the influence of the stressful experience on recovery from infection ultimately depends upon a variety of factors, including the timing of stress exposure relative to antigen/pathogen infection, specific features/parameters of the stress challenge, and the nature of the infection to which the organism has been exposed. In a now classic series of experiments, for example, Dhabhar and McEwen [1] demonstrated that exposure to acute stress facilitated some aspects of immune function, while chronic stress suppressed these same responses. Indeed, the ability of acute stress to prime certain features of the immune response and facilitate recovery from immune challenge is now well precedented [2–9]. Furthermore, it seems that stress procedures tend to increase and/or accelerate immune cell activity and cytokine expression even in the absence of antigen/pathogen exposure, therefore likely driving some of these effects. It is these more subtle, difficult to detect changes in cytokines and inflammation—evoked by the stress challenge itself—that will first be discussed in this chapter.