Weber H, Heilmann P, Meyer B, Maier K L
Gesellschaft für Strahlen- und Umweltforschung, Projekt Inhalation, Neuherberg, FRG.
FEBS Lett. 1990 Sep 17;270(1-2):90-4. doi: 10.1016/0014-5793(90)81241-f.
Cells obtained from bronchoalveolar lavage, or neutrophils of peripheral blood of dog, were incubated with the canine surfactant-associated protein A (SP-A). A significant decrease of the production of superoxide anion was observed after subsequent stimulation with phorbol-12-myristate-13-acetate (PMA) as measured by the lucigenin-dependent chemiluminescence (CL). Several other proteins used for control experiments did not decrease lucigenin-dependent CL, indicating a specific effect of SP-A on phagocytes. Treatment of SP-A with collagenase prior to incubation with neutrophils destroyed the depleting effect on oxygen radical production of PMA-stimulated cells. We propose that SP-A acts as a regulatory factor of the respiratory burst of alveolar macrophages and neutrophils in the lungs. The inhibitory effect of SP-A is down-regulated by collagenase released from stimulated alveolar macrophages.
从支气管肺泡灌洗中获取的细胞，或犬外周血中的中性粒细胞，与犬表面活性物质相关蛋白A（SP-A）一起孵育。在用佛波醇-12-肉豆蔻酸酯-13-乙酸酯（PMA）进行后续刺激后，通过光泽精依赖性化学发光（CL）测量，观察到超氧阴离子产生量显著下降。用于对照实验的其他几种蛋白质并未降低光泽精依赖性CL，表明SP-A对吞噬细胞有特定作用。在用中性粒细胞孵育之前，先用胶原酶处理SP-A，可破坏其对PMA刺激细胞氧自由基产生的消耗作用。我们提出，SP-A作为肺中肺泡巨噬细胞和中性粒细胞呼吸爆发的调节因子。SP-A的抑制作用被刺激的肺泡巨噬细胞释放的胶原酶下调。
