tate immunological memory due to elevated counts of memory and effector helper T cells (Dhabar and Viswanathan 2005).
In contrast, the innate immune response is most often enhanced in response to acute stress, including during stress conditions identical to those that interfere with specific immunity (Deak et al. 1999; Fleshner et al. 1998). A variety of stressors have been reported to increase macrophage function and elevate levels of known pro-inflammatory mediators such as interleukin-1 and tumor necrosis factor (O’Connor et al. 2003). Acute phase protein levels are similarly elevated as these cytokines also initiate the acute phase response. In addition, acute stressors potentiate or even directly elicit the sickness response, a set of behavioral and physiological changes (including fever, increased sleep, reduced social interaction and physical activity) that occur during infection (Dantzer 2004; Maier and Watkins 1998).
Chronic or repeated stress has been shown to suppress adaptive immunity (Tournier et al. 2001), but not much is known of its effects on innate immunity. Studies looking at the effects of stress on disease outcome rather than on immune responses have shown that stress can either increase or decrease disease severity depending on conditions and variables measured. Disease progression can be either inhibited or facilitated depending on the precise occurrence of the insult, as the timing of stressor exposure relative to disease onset is often critical (Johnson et al. 2006).
In addition to assays that measure T-cell proliferation, natural killer cell cytotoxicity, or B-cell activation and antibody production as indicators of adaptive immunity-stress interaction, one can also measure the capacity of polymorphonuclear cells to produce a respiratory burst in vitro. Research has shown that the functional capacity of leukocytes from stressed animals is suppressed, thus diminishing their “coping capacity” (as defined by the production of oxygen free radicals; McLaren et al. 2003).
Clinical signs interpreted through relevant animal behavior and physiological states are the most reliable distress measures. Distress evaluation is crucial when research animals are purposefully exposed to stressful conditions or when animals appear distressed unexpectedly. The assessment and subsequent interventions should involve researchers, veterinarians, and technicians and the team should continue its collaboration to develop an intervention strategy once the assessment is completed.