Experimental animal models have been used to examine stress-induced interactions among the nervous, endocrine, and immune systems. Generally, the response to stress results in a body-wide set of physiologic adaptations, mediated through the activation of neuroendocrine pathways that intersect and modulate inflammatory and immune responses. These interacting responses modulate diverse physiological processes including the initiation of tissue repair and wound healing. Two different stressors were used to activate neuroendocrine responses to study their impact on wound healing: restraint (RST) and social disruption (SDR). Previous studies showed that both stressors activate the hypothalamic-pituitary-adrenal (HPA) axis, resulting in elevated plasma levels of the corticosterone (cort) response and modulation of pro-inflammatory cytokine response. To test the effects of stress-induced HPA activation on inflammatory responses and wound healing, a 3.5-mm cutaneous punch biopsy wound was placed on the dorsal surface of control and stressed (RST or SDR) C57BL/6 male mice and the kinetics of wound healing were studied over 10 days. RST slowed wound healing in inbred C57BL/6 mice, whereas the wounds on SDR mice healed in a fashion similar to the non-stressed, home cage controls.
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