*Burn and Shock Trauma Institute, †Cell Biology, Neurobiology and Anatomy Program, ‡Immunology and Aging Program, §Stritch School of Medicine, and ∥Departments of Surgery, and ¶Microbiology and Immunology, Loyola University Chicago-Health Sciences Division, Maywood, Illinois.
Shock. 2013 Oct;40(4):327-33. doi: 10.1097/SHK.0b013e3182a43651.
This study tested the hypothesis that heightened bacterial colonization and delayed wound closure in aged mice could be attenuated by granulocyte colony-stimulating factor (G-CSF) treatment. Previously, we reported that aged mice had elevated bacterial levels, protracted wound closure, and reduced wound neutrophil accumulation after Staphylococcus aureus wound infection relative to young mice. In aseptic wound models, G-CSF treatment improved wound closure in aged mice to rates observed in young mice. Given these data, our objective was to determine if G-CSF could restore age-associated differences in wound bacterial burden and closure by increasing wound neutrophil recruitment. Young (3- to 4-month) and aged (18- to 20-month) BALB/c mice received three dorsal subcutaneous injections of G-CSF (250 ng/50 μL per injection) or saline control (50 μL per injection) 30 min after wound infection. Mice were killed at days 3 and 7 after wound infection, and bacterial colonization, wound size, wound leukocyte accumulation, and peripheral blood were evaluated. At days 3 and 7 after wound infection, bacterial colonization was significantly reduced in G-CSF-treated aged mice to levels observed in saline-treated young animals. Wound size was reduced in G-CSF-treated aged animals, with no effect on wound size in G-CSF-treated young mice. Local G-CSF treatment significantly enhanced neutrophil wound accumulation in aged mice, whereas there was no G-CSF-induced change in young mice. These data demonstrate that G-CSF enhances bacterial clearance and wound closure in an age-dependent manner. Moreover, G-CSF may be of therapeutic potential in the setting of postoperative wound infection or chronic nonhealing wounds in elderly patients.
这项研究检验了一个假设,即老年小鼠中细菌定植增加和伤口愈合延迟可以通过粒细胞集落刺激因子(G-CSF)治疗来减轻。之前,我们报道过老年小鼠在金黄色葡萄球菌伤口感染后,细菌水平升高,伤口愈合时间延长,伤口中性粒细胞积累减少,与年轻小鼠相比。在无菌性伤口模型中,G-CSF 治疗可使老年小鼠的伤口愈合速度提高到与年轻小鼠相同的水平。鉴于这些数据,我们的目的是确定 G-CSF 是否可以通过增加伤口中性粒细胞募集来恢复与年龄相关的伤口细菌负荷和愈合差异。年轻(3-4 个月)和老年(18-20 个月)BALB/c 小鼠在伤口感染后 30 分钟接受三次背部皮下注射 G-CSF(250ng/50μL/次)或生理盐水对照(50μL/次)。在伤口感染后第 3 天和第 7 天处死小鼠,评估细菌定植、伤口大小、伤口白细胞积累和外周血。在伤口感染后第 3 天和第 7 天,G-CSF 治疗的老年小鼠的细菌定植显著减少,达到生理盐水治疗的年轻动物的水平。G-CSF 治疗的老年动物的伤口大小减小,而 G-CSF 治疗的年轻动物的伤口大小没有变化。局部 G-CSF 治疗显著增强了老年小鼠的中性粒细胞伤口积累,而年轻小鼠则没有 G-CSF 诱导的变化。这些数据表明,G-CSF 以年龄依赖的方式增强细菌清除和伤口愈合。此外,G-CSF 可能在老年患者术后伤口感染或慢性不愈合伤口的治疗中有潜在的治疗价值。