Cantharidin skin blisters were examined over two days to model the acute and resolving phases of inflammation in human skin. Four blisters were created by topical administration of cantharidin (0.1% v/v) to the forearm of healthy volunteers, with IRB approval. Duplicate skin blisters were aspirated at 16 and 40 hours to model the proinflammatory and resolving phases, respectively. There was a significant increase in leukocyte infiltrate at 40?h with appearance of a “resolving macrophage” phenotype CD14+CD163+ by flow cytometry. Neutrophils acquired apoptotic markers at 40?h and were observed to be phagocytosed by macrophagic “Reiter’s” cells. Multiplex cytokine analysis demonstrated that monocyte chemoattractant protein (MCP-1/CCL2), interleukin- (IL-) 6, IL-8/CXCL8, macrophage inflammatory protein (MIP1?/CCL3), MIP-1?/CCL4, tumor necrosis factor- (TNF-) ?, and eotaxin (CCL11) were all significantly upregulated at 16?h compared with 40?h. In contrast, immunoregulatory transforming growth factor- (TGF-) ?, macrophage-derived chemokine (MDC/CCL22), and interferon-inducible protein (IP-10/CXCL10) were significantly elevated at 40?h. Our results demonstrate that the phases of inflammation and resolution can be discriminated in a two-day model of dermal wound healing. This confirms and extends our understanding of wound repair in humans and provides a powerful research tool for use in clinical settings and to track the molecular benefits of therapeutic intervention.