Dopamine is a catecholaminergic neurotransmitter which regulates several functions of the nervous, endocrine and immune systems. In the skin, dopamine would modulate keratinocytes and tissue macrophages activities. These cells are strongly involved in the cutaneous immune system defense. Against external agents, keratinocytes and macrophages of cutaneous immune system produce, proinflammatory cytokines and metalloproteinases (MMP), which can participate in wound repair process. The expression of these inflammatory mediators is regulated by several signal transduction pathways, such as the activation of NFκB, which is an important proinflammatory transcription factor expressed in many cell types, including macrophages and keratinocytes. Both cells have catecholaminergic system, which is involved in inflammatory diseases and skin physiological processes (wound healing). Previously, we demonstrated that dopaminergic agonists can stimulate keratinocytes to produce IL-6 and IL-8 which are related to inflammatory cutaneous processes. These effects are mediated by dopaminergic and β-adrenergic receptors and by receptor-independent oxidative mechanisms. In this work, we evaluated the effect of dopamine (10-6, 10-5, 10-4M) in the presence/absence of the β-adrenergic antagonist propranolol (10-5M) on wound closure (wound scratch assay), MMP activity (MMP-9, zymography), cytokine production (IL-8, IL-1β, ELISA), IκB/NFκB pathway activation (western blot), in a line of human keratinocyte HaCaT and THP-1 PMA-differentiated macrophages. We previously demonstrated that DA increased IL-6 and IL-8 production by β- adrenergic receptor in human keratinocytes. In this work, we demonstrated that DA (10-5) did not modify the wound closure in keratinocytes, but decreased the propranolol stimulatory effect (p<0.05), delaying cell migration. MMP-9 activity (p<0.001) and the propranolol-induced MMP9 activity were decreased by DA (p<0.05). In addition, DA (10-5) increase NFκB-p65 levels in nuclear extracts (p<0.01), this effect was reduced in presence of propranolol (p<0.05), suggesting NFκB pathway is involved in the DA effect on keratinocytes. On the other hand, DA (10-5) increased the MMP-9 activity (p<0.01) without alter the propranolol-induced MMP-9 activity in THP-1 macrophages. DA increased IL-8 production (p<0.01), that effect was reduced in presence of propranolol (p<0.05). However, DA did not modify NFκB-p65 in nuclear extracts, meaning that this route would not be involved in the DA effect in human macrophages. In conclusion, these results suggest a differential effect of DA via β-adrenergic receptors, depend on the physiological condition and the cell type involved, which could contribute to interfere with the wound healing process. The latter phenomenon is worth considering when novel therapeutic targets are developed for the treatment of skin diseases exacerbated by either stress conditions or infections.