Lung Immunology Group, Department of Internal Medicine/Respiratory Medicine and Allergology, Institute of Medicine, Sahlgrenska Academy at the University of Gothenburg, Guldhedsgatan 10A, Box 480, 405 30, Gothenburg, Sweden.
Inflammation. 2011 Feb;34(1):1-9. doi: 10.1007/s10753-010-9201-8.
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.
现在有大量证据表明细胞因子白细胞介素-17 协调哺乳动物中性粒细胞的积累，从而有助于宿主防御。然而，IL-17 控制中性粒细胞更新的作用尚未完全阐明。在这里，我们证明 IL-17 刺激小鼠中性粒细胞的凋亡，同时释放杀菌化合物髓过氧化物酶。IL-17 还刺激小鼠巨噬细胞吞噬衰老的中性粒细胞和乳胶珠，并诱导吞噬受体凝集素样氧化低密度脂蛋白受体-1 的可溶性形式增加。相比之下，IL-17 不会显著增加小鼠巨噬细胞中典型中性粒细胞募集细胞因子巨噬细胞炎性蛋白-2 的释放。重要的是，IL-17 还刺激人单核细胞来源的巨噬细胞对乳胶珠的吞噬作用。因此，IL-17 有可能在宿主防御激活期间控制吞噬作用和中性粒细胞更新。
