期刊
INFLAMMATION
卷 34, 期 1, 页码 1-9出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-010-9201-8
关键词
phagocytosis; apoptosis; interleukin-17; macrophages; neutrophils
资金
- Swedish Heart-Lung Foundation [20070471]
- Swedish Science Council [K2008-57X-09048-19-3]
- University of Gothenburg
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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