Acute Laboratory Stressors 1 Animal Research

Animal researchers have typically defined acute stressors as being relatively short in duration or consisting of relatively few exposures to a stressful stimulus. This general definition allows for numerous types of stressors differing in intensity, duration, and effects. Examples of stimuli that have been used to study the effects of acute stress on animals include aggressive confrontations, noise or bright light exposure, passive avoidance tasks, and tail shocks. Early animal studies reported decreased T cell proliferation during and following acute stress exposures concomitant with increases in levels of circulating corticosterone. Subsequent research determined that stress-related increases in corticosterone provided a mechanism through which stress could lead to suppressed immunity. However, recent research has clouded these conclusions by demonstrating that acute stressors do not always result in immunosuppression. By varying the type, severity, and duration of exposure as well as the time at which immune measures are sampled, acute stressors can result in suppressed, unaltered, or even enhanced immune system activity.

2. Human Research

Acute stress in the human literature is often defined as transient exposure to a variety of distressing or challenging laboratory tasks (e.g., mental arithmetic, speech tasks, and distressing films) or as a short-duration naturalistic event (e.g., first-time tandem parachute jumping). Despite differences in type and duration of stressors used and sampling time during or following stress exposure, research examining the immunomodulatory effects of acute stressors suggests that numbers of peripheral lymphocytes increase during and following acute stress, whereas lymphocyte proliferation to assorted mitogens is typically suppressed. Increased numbers of lymphocytes are thought to be due to a redistribution of cells from lymphoid organs into the peripheral blood. However, these cells are often immature and not fully capable of combating pathogens, thus leading to suppressed proliferation. In addition, acute stress may lead to decreased immune activity by downregulating the activity of existing cells.

Whereas lymphocyte proliferation consistently appears to be suppressed during stress, research examining the effects of acute stress on NK cell activity has yielded more inconsistent results. Some researchers have reported increased activity of NK cells during and following acute stress, whereas others have found decreased activity. Closer examination of the timing of blood samples in these studies suggests that those examining NK activity during or immediately after stress exposure found increases in activity, whereas those examining later time points found decreases in activity. In other words, NK activity may follow a biphasic pattern in response to acute stress, with initial increases in activity being followed by a subsequent decrease to levels below baseline. Increased innate immunity during acute stress may allow an individual to fight off opportunistic agents without having to mobilize the entire cascade of the acquired immune response. Simple opponent processes have been hypothesized to account for the subsequent decrease below baseline.

In summary, results of studies examining the impact of acute laboratory stressors on immunity suggest that acute stress is associated with increases in number but decreases in the functional efficacy of circulating lymphocytes. In addition, NK cell activity may follow a biphasic pattern of initial increases in activity followed by a decrease to below baseline levels upon stressor termination.

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