There is evidence that exposure to acute stress (mental or physical) modulates immune responses. Although previous research has focused on the immunosuppressive effects of stress, more recently it has become clear that acute stressor exposure can potentiate, as well as suppress, the immune system. Specifically there is evidence that acute stressor exposure stimulates many aspects of innate immunity; such as, resolution of bacterial inflammation, fever, macrophage/neutrophil nitric oxide, proinflammatory cytokines, and acute phase proteins. The stress-induced potentiation of innate immunity is an adaptive component of the "stress response". Interestingly, physical activity or exercise has also been reported to potentiate the same aspects of innate immunity that are stimulated by stress. In addition, physical activity can prevent the immunosuppressive effects of stress. Recently, we have reported that exposure to an established animal model of acute stress facilitates the resolution of an in vivo bacterial challenge. Rats exposed to inescapable tailshock stress, and challenged subcutaneously with E. coli, resolve the inflammatory response to the bacterial challenge nearly 2 days faster than non-stressed controls. Thus, given that physical activity can both stimulate aspects of innate function, and modulate the immunological consequences of acute stressor exposure, we were interested in investigating what effect physical activity would have on the stress-induced increase in the resolution of bacterial inflammation. Preliminary data suggest that physical activity, prior to exposure to an acute stressor, potentiates the stimulatory effect of stress on bacterial inflammation resolution. That is, rats that exercised prior to exposure to acute stress completely resolved the bacterial inflammation 3-4 days faster than rats exposed to either stress or exercise alone. Thus, the goal of this proposal is to characterize whether the decreased time required to resolve bacterial inflammation is due to an increase in bacterial clearance or a decrease in other inflammatory factors.

R03MH060301

1999-07-01

2000-06-30