Role of CC chemokine CCL6/C10 as a monocyte chemoattractant in a murine acute peritonitis
Role of CC chemokine CCL6/C10 as a monocyte chemoattractant in a murine acute peritonitis
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DOI：
10.1080/09629350400014172
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发表时间：
2004-10-01
影响因子：
4.6
通讯作者：
Matsukawa, A
中科院分区：
文献类型：
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作者：
LaFleur, AM;Lukacs, NW;Matsukawa, A
本研究的目的是确定CC趋化因子CCL6/C10在急性炎症中的作用。腹腔注射硫代乙醇酸盐后，小鼠腹膜CCL6水平升高，4h达高峰，48h后持续升高。中和CCL6可显著抑制巨噬细胞的侵袭(减少34-48%)，但对其他细胞类型无明显影响，且不影响其他趋化因子对单核/巨噬细胞的趋化作用。CCL6表达于外周血嗜酸粒细胞和诱导的巨噬细胞，但不表达于诱导的中性粒细胞。粒细胞耗竭小鼠的腹膜CCL6水平没有降低，其中嗜酸性粒细胞的内流明显受损。因此，CCL6似乎有助于巨噬细胞的渗透，这是独立于其他CC趋化因子的。在这种炎症模型中，嗜酸性粒细胞预先储存了CCL6，但不会在腹膜中释放CCL6。
THE aim of this study was to determine the role of CC chemokine CCL6/C10 in acute inflammation. Intraperitoneal injection of thioglycollate increased peritoneal CCL6, which peaked at 4 h and remained elevated at 48 h. Neutralization of CCL6 significantly inhibited the macrophage infiltration (34-48% reduction), but not other cell types, without decreasing the other CC chemokines known to attract monocytes/macrophages. CCL6 was expressed in peripheral eosinophils and elicited macrophages, but not in elicited neutrophils. Peritoneal CCL6 level was not decreased in granulocyte-depleted mice where eosinophil influx was significantly impaired. Thus, CCL6 appears to contribute to the macrophage infiltration that is independent of other CC chemokines. Eosinophils pre-store CCL6, but do not release CCL6 in the peritoneum in this model of inflammation.