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Impact of Interleukin-17 on Macrophage Phagocytosis of Apoptotic Neutrophils and Particles

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Abstract

There is now substantial evidence that the cytokine interleukin-17 orchestrates the accumulation of neutrophils in mammals and thereby contributes to host defense. However, the role of IL-17 in controlling neutrophil turnover is not fully understood. Here, we demonstrate that IL-17 stimulates the apoptosis of mouse neutrophils and, simultaneously, the release of the microbicidal compound, myeloperoxidase. IL-17 also stimulates mouse macrophages to phagocytose aged neutrophils and latex beads, and it induces an increase in a soluble form of the phagocytic receptor, lectin-like oxidized low-density lipoprotein receptor-1 as well. In contrast, IL-17 does not markedly increase the release of the archetype neutrophil-recruiting cytokine, macrophage inflammatory protein-2 in mouse macrophages. Importantly, IL-17 also stimulates the phagocytosis of latex beads in human monocyte-derived macrophages. Thus, IL-17 bears the potential to control both phagocytosis and neutrophil turnover during activation of host defense.

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Acknowledgements

We thank You Lu for skillful technical assistance at the animal facility. This work was supported by the Swedish Heart–Lung Foundation (Project No 20070471), the Swedish Science Council (Project No K2008-57X-09048-19-3), and the University of Gothenburg. Authors A.L., E.S. and P.G. co-own a non-provisional US patent application related to the utilization of IL-17 signaling for therapy.

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Correspondence to Elin Silverpil.

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Silverpil, E., Glader, P., Hansson, M. et al. Impact of Interleukin-17 on Macrophage Phagocytosis of Apoptotic Neutrophils and Particles. Inflammation 34, 1–9 (2011). https://doi.org/10.1007/s10753-010-9201-8

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