Wound healing in the PU.1 null mouse - Tissue repair is not dependent on inflammatory cells
Wound healing in the PU.1 null mouse - Tissue repair is not dependent on inflammatory cells
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DOI：
10.1016/s0960-9822(03)00396-8
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发表时间：
2003-07-01
期刊：
影响因子：
9.2
通讯作者：
McKercher, SR
中科院分区：
文献类型：
--
作者：
Martin, P;D'Souza, D;McKercher, SR
新生儿和成人组织的损伤总是会引起炎性中性粒细胞和巨噬细胞的流入。除了清除入侵微生物的伤口外，这些细胞被认为是修复过程的关键协调者，既作为专业吞噬细胞清除伤口碎片，又作为伤口生长因子信号的主要来源。在这里，我们报告了PU.1基因敲除小鼠的伤口愈合研究，由于缺乏巨噬细胞和功能性中性粒细胞，该小鼠在遗传上不能提高标准炎症反应。与教条相反，我们表明这些“无巨噬细胞”小鼠能够以与野生型兄弟姐妹相似的时间过程修复皮肤伤口，并且修复似乎与胚胎一样无疤痕，这也愈合了伤口而不引起炎症反应。伤口部位的生长因子和细胞因子谱改变，细胞死亡减少，并且垂死细胞反而被替代吞噬成纤维细胞吞噬。我们还表明，过度神经支配的伤口部位，以前被认为是炎症的结果，是存在于PU。1空伤口，太。
Damage to neonatal and adult tissues always incites an influx of inflammatory neutrophils and macro-m phages. Besides clearing the wound of invading microbes, these cells are believed to be crucial coordinators of the repair process, acting both as professional phagocytes to clear wound debris and as a major source of wound growth factor signals. Here we report wound healing studies in the PU.1 null mouse, which is genetically incapable of raising the standard inflammatory response because it lacks macrophages and functioning neutrophils. Contrary to dogma, we show that these "macrophageless" mice are able to repair skin wounds with similar time course to wild-type siblings, and that repair appears scar-free as in the embryo, which also heals wounds without raising an inflammatory response. The growth factor and cytokine profile at the wound site is changed, cell death is reduced, and dying cells are instead engulfed by stand-in phagocytic fibroblasts. We also show that hyperinnervation of the wound site, previously believed to be a consequence of inflammation, is present in the PU.1 null wound, too.