Zhang P, Bagby G J, Stoltz D A, Spitzer J A, Summer W R, Nelson S
Department of Medicine, Louisiana State University Medical Center, New Orleans 70112, USA.
Shock. 1997 Mar;7(3):193-9. doi: 10.1097/00024382-199703000-00007.
The effects of granulocyte colony-stimulating factor (G-CSF) on the functional activities of circulating and lung-recruited neutrophils (PMNs) and alveolar macrophages (AMs) were studied in rats to further elucidate the mechanisms underlying G-CSF-enhanced pulmonary host defense. Animals received G-CSF or vehicle twice a day for 2 days, followed by an intratracheal challenge with endotoxin or saline. G-CSF up-regulated CD11b/c expression and mean channel fluorescence intensity of phagocytosis in circulating PMNs. G-CSF also enhanced phagocytic activities, reflected by both the percentage of phagocytosis and mean channel fluorescence intensity in lung-recruited PMNs and AMs in intratracheal endotoxin-challenged rats. The endotoxin-induced increase in pulmonary production of tumor necrosis factor-alpha and cytokine-induced neutrophil chemoattractant was not affected by G-CSF pretreatment. These data demonstrate that G-CSF-enhanced pulmonary recruitment of PMNs is primarily based on the effects of G-CSF on the PMNs themselves, rather than the generation of certain chemotactic stimuli, i.e., cytokine-induced neutrophil chemoattractant and tumor necrosis factor-alpha. The enhanced phagocytic activities of lung-recruited PMNs and AMs also augment pulmonary host defenses in G-CSF-pretreated animals.
在大鼠中研究了粒细胞集落刺激因子（G-CSF）对循环和肺募集的中性粒细胞（PMN）以及肺泡巨噬细胞（AM）功能活性的影响，以进一步阐明G-CSF增强肺部宿主防御的潜在机制。动物每天接受两次G-CSF或赋形剂，持续2天，随后经气管内给予内毒素或生理盐水进行攻击。G-CSF上调循环PMN中CD11b/c的表达以及吞噬作用的平均通道荧光强度。在经气管内给予内毒素攻击的大鼠中，G-CSF还增强了肺募集的PMN和AM的吞噬活性，这通过吞噬百分比和平均通道荧光强度得以体现。内毒素诱导的肺肿瘤坏死因子-α和细胞因子诱导的中性粒细胞趋化因子产生增加不受G-CSF预处理影响。这些数据表明，G-CSF增强的PMN肺募集主要基于G-CSF对PMN自身的作用，而非某些趋化刺激物的产生，即细胞因子诱导的中性粒细胞趋化因子和肿瘤坏死因子-α。肺募集的PMN和AM增强的吞噬活性也增强了G-CSF预处理动物的肺部宿主防御。
