Inflammatory processes that occur after injury contribute to wound closure. Previous studies showed that wounds of restraint-stressed (RST) mice had a reduced number of inflammatory cells and healed more slowly compared to controls. To investigate the molecular mechanisms between stress and wound healing, we studied cutaneous gene expression of IL-1α, IL-1β, and KGF-1. Female SKH-1 mice were restrained for 3 days before and for 5 days following placement of cutaneous wounds. Wounds were subjected to competitive RT–PCR. At day 1, RST mice had significantly lower IL-1β and KGF-1 mRNA than controls. At day 5, RST mice had significantly higher IL-1α and IL-1β mRNA than controls. Treatment of RST mice with the glucocorticoid receptor antagonist RU486 restored IL-1β mRNA expression at day 1. Our results suggest that stress induces alterations in the kinetics of cutaneous proinflammatory cytokine and growth factor gene expression which could impair the quality of healing tissues.