QUANTITATIVE STUDIES OF PHAGOCYTOSIS
QUANTITATIVE STUDIES OF PHAGOCYTOSIS
复制标题
吞噬作用的定量研究
作者：
T. Stossel
本文通过人粒细胞和兔肺泡巨噬细胞对白蛋白包裹的石蜡油粒的初始摄取率的动力学分析，研究了阳离子和热不稳定调理素对吞噬的作用机制。Ca++、Mg++、Mn++或Co++对颗粒的摄取速率有促进作用。高浓度(>；20 mM)的Ca~(++)和Mg~(++)抑制摄食率。用新鲜血清(不耐热的调色素)处理这些颗粒也会刺激摄取率。~(125)I标记的C3在调理过程中被结合到粒子上。缺乏C3的人血清缺乏调理活性，通过添加纯化的C3恢复了调理活性。正常、C2缺陷和遗传性血管神经性水肿血清具有相同的调理活性。因此，血清的调理活性与补体蛋白系统对颗粒的C3结合有关。虽然镁离子和不耐热的调色素都加速了颗粒的最大摄取率，但两者都没有改变与一半最大摄取率相关的颗粒浓度。颗粒的调理显着降低了二价阳离子的浓度，对摄取率有促进作用和抑制作用，并改变了阳离子活化曲线的形状。~(45)Ca在调理过程中未与颗粒结合。结果与二价阳离子和热不稳定调理素通过刺激吞噬功而不是仅仅通过增强细胞-颗粒亲和力来激活摄取的机制是一致的，而热不稳定调理素通过加强二价阳离子的影响而起作用。
Kinetic analysis of the initial ingestion rate of albumin-coated paraffin oil particles by human granulocytes and rabbit alveolar macrophages was undertaken to study the mechanism of action of cations and of heat-labile opsonin on engulfment. The rate of uptake of the particles was stimulated by Ca++, Mg++, Mn++, or Co++. At high concentrations (> 20 mM) Ca++ and Mg++ inhibited the rate of ingestion. Treatment of the particles with fresh serum (heat-labile opsonin) also stimulated the rate of ingestion. 125I-labeled C3 was bound to the particles during opsonization. C3-deficient human serum lacked opsonic activity, which was restored by addition of purified C3. Normal, C2-deficient, and hereditary angioneurotic edema sera had equivalent opsonic activity. The serum opsonic activity thus involved C3 fixation to the particles by means of the properdin system. Although Mg++ and heat-labile opsonin both accelerated the maximal rates of ingestion of the particles, neither altered the particle concentrations associated with one-half maximal ingestion rates. Opsonization of the particles markedly diminished the concentrations of divalent cations causing both stimulatory and inhibitory effects on ingestion rates and altered the shapes of the cation activation curves. 45Ca was not bound to the particles during opsonization. The results are consistent with a mechanism whereby divalent cations and heat-labile opsonin activate ingestion by stimulating the work of engulfment rather than by merely enhancing cell-particle affinity, and whereby heat-labile opsonin acts by potentiating the effects of divalent cations.