Social interactions, stress, and immunity

Abstract

This review summarizes the endocrine and immune changes induced by an experimental model for social stress that is termed SDR. Further, the differences between this stressor and other chronic stress models in mice are compared and contrasted. Individual differences in the response to SDR are described and discussed in the context of the unique characteristics of this stressor and the importance of a variety of behavioral and environmental factors in modulating the response to social stress. The collection of data indicates that mice facing a social stressor may use different behavioral coping responses based on the environmental conditions and previous experiences. These different adaptational responses are reflected in their behavioral, endocrine, and immune changes in response to the stressor [7], [8]. In conclusion, although generally it is understood that chronic stressors suppress immune function and increase a host's susceptibility to disease, this may not be dogma. For example, under conditions in which individuals face the chance of being injured, which may be a chronic or reoccurring likelihood, it may be an adaptive advantage to maintain or even enhance an immune response. The development of GCR after SDR may be such a mechanism, allowing animals to heal injuries and clear invading bacteria in the presence of the anti-inflammatory stress hormones. Thus, individual differences in response to SDR are associated with specific behavioral strategies that can have substantive implications for host resistance to infectious disease.