Gemmell C G, O'Dowd A
J Antimicrob Chemother. 1983 Dec;12(6):587-97. doi: 10.1093/jac/12.6.587.
Protein A, a component of the outer layer of the cell wall of Staphylococcus aureus impairs opsonization by serum complement and thereby delays phagocytosis by polymorphonuclear leukocytes. Two antibiotics with modes of action on bacterial protein biosynthesis, have been used at sub-growth inhibitory concentrations to regulate the production of protein A. Both clindamycin and fusidic acid (either at 1/2 or 1/4 MIC) reduced the amount of protein A on the cell surface. Such drug-grown cells became more susceptible to phagocytic uptake and killing. Chemiluminescence (CL) of PMN when presented with preopsonized drug-grown staphylococci was potentiated and correlated with the enhanced phagocytosis seen earlier. The level of CL appeared to depend upon the amount of human serum used to opsonize the bacteria. Reduced protein A content on the cell surface probably resulted in the exposure of a greater number of receptor sites for C3b, rendering the bacterium more susceptible to attachment and ingestion by the polymorphonuclear leukocyte.
蛋白A是金黄色葡萄球菌细胞壁外层的一种成分,它会削弱血清补体的调理作用,从而延迟多形核白细胞的吞噬作用。两种对细菌蛋白质生物合成有作用方式的抗生素,已在亚生长抑制浓度下使用,以调节蛋白A的产生。克林霉素和夫西地酸(均为1/2或1/4 MIC)都减少了细胞表面蛋白A的量。这种经药物处理生长的细胞对吞噬摄取和杀伤变得更敏感。当用预调理的经药物处理生长的葡萄球菌刺激时,多形核白细胞的化学发光(CL)增强,且与早期观察到的吞噬作用增强相关。CL的水平似乎取决于用于调理细菌的人血清量。细胞表面蛋白A含量的减少可能导致更多C3b受体位点的暴露,使细菌更容易被多形核白细胞附着和摄取。