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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >The chemotaxis of M1 and M2 macrophages is regulated by different chemokines
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The chemotaxis of M1 and M2 macrophages is regulated by different chemokines

机译：M1和M2巨噬细胞的趋化性受不同趋化因子的调节

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摘要

The homing of proinflammatory (M1) and the "alternatively activated" anti-inflammatory (M2) macrophages plays a different role in the process of inflammation. Chemokines are the major mediators of macrophage chemotaxis, but how they differentially regulate M1 and M2 macrophages remains largely unclear. In the present study, we attempted to screen chemokines that differentially induce chemotaxis of M1 and M2 macrophages and to explore the underlying mechanism. Among the 41 chemokines that specifically bind to 20 chemokine receptors, CCL19, CCL21, CCL24, CCL25, CXCL8, CXCL10, and XCL2 specifically induced M1 macrophage chemotaxis, whereas CCL7 induced chemotaxis of both M1 and M2 macrophages. Whereas the differential effects of these chemokines on M1/M2 macrophage chemotaxis could be attributable to the predominant expression of their cognate receptors on the macrophage subsets, CCR7, the receptor for CCL19/CCL21, appeared to be an exception. Immunoblot analysis indicated an equivalent level of CCR7 in the whole cell lysate of M1 and M2 macrophages, but CCL19 and CCL21 only induced M1 macrophage chemotaxis. Both immunoblot and confocal microscopy analyses demonstrated that CCR7 was predominantly expressed on the cell surface of M1 but in the cytosol of M2 macrophages before ligand stimulation. As a result, CCL19 or CCL21 induced activation of both MEK1-ERK1/2 and PI3K-AKT cascades in M1 but not in M2 macrophages. Intriguingly, CCL19/CCL21-mediated M1 macrophage chemotaxis was blocked by specific inhibition of PI3K rather than MEK1. Together, these findings suggest that recruitment of M1 and M2 macrophages is fine tuned by different chemokines with the involvement of specific signaling pathways.
机译：促炎（M1）和“另类激活的”抗炎（M2）巨噬细胞的归巢在炎症过程中起着不同的作用。趋化因子是巨噬细胞趋化性的主要介质，但是它们如何差异调节M1和M2巨噬细胞仍不清楚。在本研究中，我们试图筛选差异诱导M1和M2巨噬细胞趋化性的趋化因子，并探索其潜在机制。在特异性结合20种趋化因子受体的41种趋化因子中，CCL19，CCL21，CCL24，CCL25，CXCL8，CXCL10和XCL2特异性诱导M1巨噬细胞趋化性，而CCL7诱导M1和M2巨噬细胞趋化性。这些趋化因子对M1 / M2巨噬细胞趋化性的不同影响可能归因于它们在巨噬细胞亚群上的同源受体的主要表达，CCR7（CCL19 / CCL21的受体）似乎是一个例外。免疫印迹分析表明，在M1和M2巨噬细胞的全细胞裂解物中，CCR7的水平相同，但CCL19和CCL21仅诱导M1巨噬细胞的趋化性。免疫印迹和共聚焦显微镜分析均表明，在配体刺激之前，CCR7主要在M1的细胞表面表达，但在M2巨噬细胞的胞浆中表达。结果，CCL19或CCL21诱导了M1巨噬细胞中MEK1-ERK1 / 2和PI3K-AKT级联的激活。有趣的是，CCL19 / CCL21介导的M1巨噬细胞趋化性被PI3K而非MEK1的特异性抑制所阻断。在一起，这些发现表明，M1和M2巨噬细胞的募集是由不同的趋化因子在特定信号通路的参与下进行微调的。

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