Vazifeh D, Preira A, Bryskier A, Labro M T
INSERM U 479, Laboratoire d'Hématologie et Immunologie, CHU X. Bichat, 75018 Paris, France.
Antimicrob Agents Chemother. 1998 Aug;42(8):1944-51. doi: 10.1128/AAC.42.8.1944.
HMR 3647, a new ketolide, is active upon intracellular pathogens. We previously demonstrated that HMR 3004 (RU 64004), another ketolide, is highly concentrated by human polymorphonuclear neutrophils (PMNs). This prompted us to evaluate whether the presence of a 3-keto group instead of an L-cladinose, a neutral sugar characteristic of erythromycin A derivatives, confers peculiar pharmacokinetic properties with regard to cellular accumulation and efflux. After incubation with the radiolabelled drug, HMR 3647 uptake was determined by a velocity gradient centrifugation technique. HMR 3647 was avidly concentrated by PMNs, without saturation, over a 3-h incubation period, with cellular-to-extracellular concentration ratios of 31 +/- 4.2 at 5 min and up to 348 +/- 27.1 at 180 min. About 60% of HMR 3647 was located in the granular compartment; less than 6% was associated with the membranes. HMR 3647 gradually egressed from loaded cells placed in drug-free medium. Uptake was dependent on environmental temperature (activation energy, 128 +/- 9. 4 kJ/mol) but not on extracellular pH. HMR 3647 displayed Michaelis-Menten saturation kinetics with a mean Vmax of 2315 ng/2.5 x 10(6) PMNs/5 min and a mean Km of 117 mg/liter (144 microM). As already observed with erythromycin A-derived macrolides, extracellular Ca2+ was necessary for optimal uptake of HMR 3647. Interestingly, verapamil increased the uptake of HMR 3647 at 5 min, but this was followed by gradual inhibition at later incubation times, a phenomenon probably related to stimulation of drug efflux. The impact of intracellular accumulation of HMR 3647 on PMN functions was also investigated. In contrast to other erythromycin A derivatives, HMR 3647 only weakly triggered granule exocytosis, but it inhibited superoxide anion production in a time- and concentration-dependent manner, with concentrations which inhibited 50% of control response of 55 (67 microM) (5 min) and 30 (36 microM) (30 min) mg/liter for formyl-methionyl-leucyl-phenylalanine stimulation and 117 (143 microM) (5 min) and 44 (54 microM) (30 min) mg/liter for phorbol myristate acetate stimulation.
新型酮内酯类药物HMR 3647对细胞内病原体具有活性。我们之前证明了另一种酮内酯类药物HMR 3004(RU 64004)可被人多形核中性粒细胞(PMN)高度浓缩。这促使我们评估3-酮基取代了红霉素A衍生物特有的中性糖L-克拉定糖后,在细胞摄取和外排方面是否赋予了独特的药代动力学特性。用放射性标记药物孵育后,通过速度梯度离心技术测定HMR 3647的摄取量。在3小时的孵育期内,PMN可大量摄取HMR 3647且无饱和现象,5分钟时细胞内与细胞外浓度比为31±4.2,180分钟时高达348±27.1。约60%的HMR 3647位于颗粒区室;与细胞膜相关的不到6%。HMR 3647从置于无药培养基中的负载细胞中逐渐排出。摄取取决于环境温度(活化能,128±9.4 kJ/mol),但不取决于细胞外pH值。HMR 3647表现出米氏饱和动力学,平均Vmax为2315 ng/2.5×10⁶ PMN/5分钟,平均Km为117 mg/升(144 μM)。正如红霉素A衍生的大环内酯类药物所观察到的那样,细胞外Ca²⁺是HMR 3647最佳摄取所必需的。有趣的是,维拉帕米在5分钟时增加了HMR 3647的摄取,但在随后的孵育时间里逐渐受到抑制,这种现象可能与药物外排的刺激有关。还研究了HMR 3647在细胞内蓄积对PMN功能的影响。与其他红霉素A衍生物不同,HMR 3647仅微弱地触发颗粒胞吐作用,但它以时间和浓度依赖性方式抑制超氧阴离子的产生,对于甲酰甲硫氨酰亮氨酰苯丙氨酸刺激,抑制50%对照反应的浓度为55(67 μM)(5分钟)和30(36 μM)(30分钟)mg/升,对于佛波酯刺激,抑制50%对照反应的浓度为117(143 μM)(5分钟)和44(54 μM)(30分钟)mg/升。