The transition from neutrophil to mononuclear-cell infiltrate is a hallmark of acute inflammation. The kinetics of leuko-endothelial adhesion molecule expression and chemokine secretion might participate in the initial recruitment of neutrophils. Neutrophils then die in situ by apoptosis, while mononuclear cells accumulate. We propose that interleukin-6 (IL-6) and its soluble receptor (sIL-6Rα) might regulate the leukocyte recruitment transition, through a shift of chemokine production. This new function of IL-6 might aid in the understanding of its complex role in inflammation: during acute inflammation, IL-6 might favor the resolution of the neutrophilic infiltrate and the initiation of the immune response; in chronic inflammation, IL-6 might increase the mononuclear-cell infiltrate and participate in disease pathogenesis.