Both exposure to positive social interactions and stress can influence health outcome, via alterations in the hypothalamic-pituitary-adrenal (HPA) axis and changes in immune functioning. The first series of experiments examined the roles of social interactions and stress on wound healing and HPA axis activity in Peromyscus species exhibiting various social structures. Social facilitation decreased wound size in male monogamous versus male polygamous Peromyscus; this relationship was mediated by physical contact. Further investigation of social facilitation and stress effects on wound healing elucidated the interactions between pair housing and wound healing by examining various housing dyads. Positive social interactions facilitate wound healing in monogamous and polygynous Peromyscus regardless of the sex of the experimental or stimulus mouse. However, the effects of pair housing on wound healing are limited; male and female polygynous mice benefit from pair housing, but only under non-stressed conditions. Thus, differences in social systems can influence the extent to which social interactions may be beneficial to wound healing.
The second series of experiments examined the impact of endogenous glucocorticoids on physiological parameters following experimental stroke. Stress exacerbates post-stroke neuronal damage, via increases in circulating corticosteroid concentrations and greater cerebral edema, compared to mice not experiencing stress or those allowed a temporal window between the conclusion of stress and the onset of stroke.
The third series of experiments examined the effects of experimental stroke on peripheral immune function. An augmentation in the peripheral immune response is observed following stroke; however, stroke failed to alter the rate of cutaneous wound healing. This augmentation in peripheral immune function was mitigated when neuronal damage was prevented via hypothermia. Pair housing also mitigated the effects of stroke on cell-mediated immune function and reduced wound size, regardless of the surgical condition. Restraint stress increases neuronal damage, which can lead to a decrease in humoral immune function when coupled with stress following stroke; however, stress, in the absence of neuronal damage, increases humoral immune function, thereby further adding to the literature elucidating stress effects on immune function. In conclusion, the work described in this dissertation adds to the body of literature that elucidates the relationship between social interactions, stress, and health.