Sakai K, Kweon M N, Kohri T, Kishino Y
Department of Nutrition, School of Medicine, University of Tokushima, Japan.
Cell Mol Biol. 1992 Apr;38(2):123-30.
Pulmonary surfactant isolated from bronchoalveolar lavage fluid of rat lung contained a high content of surfactant protein A (SP-A) in starved for 2 days compared to fed controls, but this phenomena returned to baseline following more than 4 days starvation. As determined by immunoperoxidase staining of lung sections using SP-A antibody, SP-A could be consistently observed in nonciliated bronchiolar (Clara) cells, alveolar type II cells and some alveolar macrophages (AM). Fc receptor-mediated phagocytosis of AM was enhanced by SP-A, which was dependent on the dosis and reached a maximum at 10 micrograms of SP-A/ml. Antibody to SP-A completely inhibited the enhanced response of phagocytosis. When exposed AM subpopulations, separated into four fractions (I, II, III and IV) by discontinuous Percoll gradient, to SP-A or pulmonary surfactant prepared from rats fed and starved for 2 days enhanced their phagocytic activity in high dense cells (III and IV), particularly to SP-A and pulmonary surfactant from rats starved for 2 days. Whereas little change in lower dense fractions (I and II) were seen in all exposures except for SP-A that enhanced the cells of fraction II. These results supported the concept that pulmonary surfactant and its apoprotein, SP-A, are a factor to regulate lung defense system including activation of AM that undergo different processes following starvation.
与喂食对照组相比,从饥饿2天的大鼠肺支气管肺泡灌洗液中分离出的肺表面活性物质含有高含量的表面活性蛋白A(SP-A),但饥饿超过4天后,这种现象恢复到基线水平。通过使用SP-A抗体对肺切片进行免疫过氧化物酶染色确定,在无纤毛细支气管(克拉拉)细胞、II型肺泡细胞和一些肺泡巨噬细胞(AM)中可始终观察到SP-A。SP-A可增强AM的Fc受体介导的吞噬作用,这取决于剂量,在10微克SP-A/毫升时达到最大值。SP-A抗体完全抑制吞噬作用的增强反应。当将通过不连续Percoll梯度分离成四个部分(I、II、III和IV)的AM亚群暴露于SP-A或由喂食和饥饿2天的大鼠制备的肺表面活性物质时,高密度细胞(III和IV)中的吞噬活性增强,特别是对饥饿2天的大鼠的SP-A和肺表面活性物质。除了SP-A增强了II部分的细胞外,在所有暴露中低密度部分(I和II)几乎没有变化。这些结果支持了这样的概念,即肺表面活性物质及其载脂蛋白SP-A是调节肺防御系统的一个因素,包括激活饥饿后经历不同过程的AM。