Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
Division of Inflammation Biology, Tokushima University, Tokushima 7708503, Japan.
Science. 2017 Oct 6;358(6359):111-116. doi: 10.1126/science.aam9690.
Neutrophils have been implicated as harmful cells in a variety of inappropriate inflammatory conditions where they injure the host, leading to the death of the neutrophils and their subsequent phagocytosis by monocytes and macrophages. Here we show that in a fully repairing sterile thermal hepatic injury, neutrophils also penetrate the injury site and perform the critical tasks of dismantling injured vessels and creating channels for new vascular regrowth. Upon completion of these tasks, they neither die at the injury site nor are phagocytosed. Instead, many of these neutrophils reenter the vasculature and have a preprogrammed journey that entails a sojourn in the lungs to up-regulate CXCR4 (C-X-C motif chemokine receptor 4) before entering the bone marrow, where they undergo apoptosis.
中性粒细胞已被认为是多种不当炎症情况下有害的细胞,在这些情况下,它们会伤害宿主,导致中性粒细胞死亡,随后被单核细胞和巨噬细胞吞噬。在这里,我们发现,在完全修复无菌性热肝损伤的过程中,中性粒细胞也会渗透到损伤部位,并完成拆卸受损血管和为新血管再生创造通道的关键任务。完成这些任务后,它们既不会在损伤部位死亡,也不会被吞噬。相反,许多这些中性粒细胞重新进入血管系统,并进行预先编程的旅程,包括在肺部停留以上调 CXCR4(C-X-C 基序趋化因子受体 4),然后进入骨髓,在那里它们会凋亡。