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Role of CC chemokine CCL6/C10 as a monocyte chemoattractant in a murine acute peritonitis.

机译:CC趋化因子CCL6 / C10在鼠急性腹膜炎中作为单核细胞趋化因子的作用。

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摘要

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.
机译:这项研究的目的是确定CC趋化因子CCL6 / C10在急性炎症中的作用。腹腔注射巯基乙酸盐可增加腹膜CCL6,其在4 h达到峰值,并在48 h保持升高。 CCL6的中和作用显着抑制了巨噬细胞的浸润(减少了34-48%),但没有抑制其他类型的细胞,却没有降低已知吸引单核细胞/巨噬细胞的其他CC趋化因子。 CCL6在周围的嗜酸性粒细胞和诱发的巨噬细胞中表达,但在诱发的嗜中性粒细胞中不表达。在嗜酸性粒细胞流入明显受损的粒细胞缺乏小鼠中,腹膜CCL6水平没有降低。因此,CCL6似乎有助于巨噬细胞浸润,而独立于其他CC趋化因子。嗜酸性粒细胞可预先储存CCL6,但在这种炎症模型中不会在腹膜中释放CCL6。

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