Cellulitis has long been postulated to be the result of antecedent bacterial invasion with subsequent bacterial proliferation. Nonetheless, the difficulty in isolating putative pathogens from cellulitic skin has served to cast doubt on this hypothesis. In this regard, the skin is provided with a unique set of lymphoid and reticular cells with the capacity to secrete lymphokines and cytokines. These substances rapidly reduce the number of viable bacteria from infection by enhancing the infiltration of skin by circulating macrophages and neutrophils. The warmth and erythema associated with cellulitis are most likely produced both by a small number of residual bacteria and by fragmented bacterial remnants, and amplified by the lymphokines that are secreted in response to antigenic challenge. Anti-inflammatory agents may play a significant role in enhancing the resolution of infection by reducing the production of soluble mediators by these intra-epidermal immunocompetent cells.