Inserm, Institut national de la santé et de la recherche médicale
Faculté de pharmacie, Aix Marseille Université

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Interleukin-6 : a regulator of the transition from neutrophilic to monocytic inflammation

G. Kaplanski, V. Marin, F. Montero-Julian, A. Mantovani, C. Farnarier. Trends in Immunology, 2003, 24 : 25-29.


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.
Inflammation is a complex defense mechanism characterized by leukocyte migration from the vasculature into damaged tissues to destroy the injurious agents. Acute inflammation is a limited beneficial response particularly during infectious challenges, whereas chronic inflammation is a persistent phenomenon, which can progress to inflammatory diseases. One hallmark of acute inflammation is that the leukocyte infiltrate is initially mostly neutrophilic but after 24 to 48 h, monocytic cells predominate 1, 2 and 3. By contrast, chronic inflammation is histologically associated with the presence of mononuclear cells, such as macrophages and lymphocytes 1 and 2. Although several explanations have been suggested, the mechanisms controlling the transition from neutrophil to monocyte recruitment during acute inflammation are poorly known. Here, we review different possible mechanisms involved and propose that the IL-6–soluble IL-6Rα (sIL-6Rα) complex might have an important role in this transition.