巨噬细胞是我们机体中强大的“吃豆小精灵”，其可以吞咽细胞残渣及病原体来保护机体健康，近日，一篇刊登在国际杂志The Journal of Cell BioLogy上的研究论文中，来自威斯康辛-迈迪逊大学大学的研究人员揭示了巨噬细胞如何通过诱导中性白细胞，使其离开机体损伤的组织进而帮助治疗炎症。

中性粒细胞是机体中的“第一急救者”，其可以被名为活性氧激活的蛋白激酶所吸引到患处，当中性粒细胞完成工作后，炎症就会通过细胞自杀或凋亡的方式被部分治疗，随后残留的中性粒细胞就会被巨噬细胞所吞噬;但中性粒细胞可以通过一种逆向迁移的方式离开机体损伤的组织，目前是否巨噬细胞可以促进炎症的恢复尚不明确。

这项研究中，研究人员利用透明的斑马鱼幼体进行研究，结果发现，在被巨噬细胞吞噬前中性粒细胞会被“招募”至伤口处，但是一旦其到达伤口处，巨噬细胞就会同中性粒细胞进行接触，并且使其远离机体损伤组织;在缺失巨噬细胞的斑马鱼机体中中性粒细胞可以在斑马鱼患处停留很长时间。就像中性粒细胞一样，巨噬细胞可以被活性氧和蛋白激酶信号吸引至患处，而且缺失活性氧产生酶类Nox2的巨噬细胞并不能迁移至伤口处，反而会诱导中性粒细胞离开伤口。

更有意思的是，研究人员发现，缺失人类等量Nox2的病人往往会遭受感染的复发及炎性的扩展，这种障碍名为慢性肉芽肿病;本文研究揭示了一种引发病人患慢性肉芽肿病的原因或许是因为机体巨噬细胞并不能迁移到炎性位点来诱导中性粒细胞的反向迁移活动及炎性的恢复。
 

原文：Redox and Src family kinase signaling control leukocyte wound attraction and neutrophil reverse migration

原文摘要：Tissue damage induces early recruitment of neutrophils through redox-regulated Src family kinase (SFK) signaling in neutrophils. Redox-SFK signaling in epithelium is also necessary for wound resolution and tissue reGENEration. How neutrophil-mediated inflammation resolves remains unclear. In this paper, we studied the interactions between macrophages and neutrophils in response to tissue damage in zebrafish and found that macrophages contact neutrophils and induce resolution via neutrophil reverse migration. We found that redox-SFK signaling through p22phox and Yes-related kinase is necessary for macrophage wound attraction and the subsequent reverse migration of neutrophils. Importantly, macrophage-specific reconstitution of p22phox revealed that macrophage redox signaling is necessary for neutrophil reverse migration. Thus, redox-SFK signaling in adjacent tissues is essential for coordinated leukocyte wound attraction and repulsion through pathways that involve contact-mediated guidance.

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