Steinberg T H, Hand W L
J Infect Dis. 1984 Mar;149(3):397-403. doi: 10.1093/infdis/149.3.397.
The ability of antibiotics to enter phagocytes during infection with facultative intracellular organisms was investigated using an in vitro model. Human polymorphonuclear leukocytes (PMNLs) were incubated with ingestible particles or phorbol myristate acetate (PMA), after which radiolabeled antibiotics were added to the cell suspension. Antibiotic uptake, determined by a velocity-gradient centrifugation technique, was expressed as the cellular:extracellular (C/E) antibiotic concentration ratio. Phagocytosis or PMA exposure enhanced PMNL clindamycin uptake (for example, C/E ratio of 12 for control vs 30 after zymosan). Entry of penicillin was unaffected and erythromycin uptake was slightly decreased after phagocytosis. Because clindamycin uptake by phagocytes is mediated by the nucleoside transport system, adenosine uptake after phagocytosis was studied. Adenosine uptake was stimulated by phagocytosis, and this increase was inhibited by clindamycin. Thus, clindamycin uptake, mediated by the nucleoside transport system, was augmented by phagocytosis. This marked stimulation of a membrane transport system by phagocytosis has not been previously described.
利用体外模型研究了在兼性胞内菌感染期间抗生素进入吞噬细胞的能力。将人类多形核白细胞（PMNLs）与可摄取颗粒或佛波酯（PMA）一起孵育，之后将放射性标记的抗生素添加到细胞悬液中。通过速度梯度离心技术测定的抗生素摄取量，以细胞内：细胞外（C/E）抗生素浓度比表示。吞噬作用或PMA暴露增强了PMNL对克林霉素的摄取（例如，对照组的C/E比为12，经酵母聚糖处理后为30）。吞噬作用后青霉素的进入不受影响，红霉素的摄取略有下降。由于吞噬细胞对克林霉素的摄取是由核苷转运系统介导的，因此研究了吞噬作用后腺苷的摄取。吞噬作用刺激了腺苷摄取，而这种增加被克林霉素抑制。因此，由核苷转运系统介导的克林霉素摄取因吞噬作用而增强。吞噬作用对膜转运系统的这种显著刺激此前尚未见报道。
