Accumulation of rifampicin by Mycobacterium aurum, Mycobacterium smegmatis and Mycobacterium tuberculosis.
Accumulation of rifampicin by Mycobacterium aurum, Mycobacterium smegmatis and Mycobacterium tuberculosis.
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金黄色分枝杆菌、耻垢分枝杆菌和结核分枝杆菌积累利福平。
DOI：
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发表时间：
2000
影响因子：
5.2
通讯作者：
V. Ricci
中科院分区：
文献类型：
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作者：
L. Piddock;K. Williams;V. Ricci
测定了野生型金黄分枝杆菌（A（+））、耻垢分枝杆菌（mc（2）155）和结核分枝杆菌（H37 Rv）对2 mg/L [（14）C]利福平的蓄积特性。暴露10 min后，M. aurum积累利福平220 ng/mg细胞，M.结果表明，在120 ng/mg细胞的利福平浓度下，M.结核病累积了154 ng利福平/mg细胞。利福平在M. aurum和M.与M. smeglavin，它积累利福平更慢。随着利福平浓度从0.12 mg/L增加到2 mg/L，M.结核病，在积累实验的20分钟内没有可检测到的活力损失。随着温度的升高，M.结核病;在15和30摄氏度之间，增加是线性的。对于所有三个物种亚抑制浓度的乙胺丁醇增加利福平的浓度积累。然而，在0.05%吐温80存在下，利福平的生长和积累均较低。利福平在M.无论是在将利福平加入分枝杆菌培养物之前还是之后加入质子动力抑制剂2，4-二硝基苯酚（1 mM），均不影响斯美加。革兰氏阳性菌外排抑制剂利血平（20 mg/L）对所有3种菌的利福平SSC均有轻微增加，但增加幅度无统计学意义。在利血平存在或不存在的情况下，添加葡萄糖以激发假定的外排泵对利福平的蓄积几乎没有影响。结核病，而M. aurum和M.加葡萄糖可消除利血平的作用。这些数据表明，利福平可以通过外排从野生型分枝杆菌中去除，但泵的表达水平较低。
The characteristics of the accumulation of 2 mg/L [(14)C]rifampicin by wild-type strains of Mycobacterium aurum (A(+)), Mycobacterium smegmatis (mc(2)155) and Mycobacterium tuberculosis (H37Rv) were determined. After 10 min exposure M. aurum had accumulated 220 ng rifampicin/mg cells, M. smegmatis had accumulated 120 ng rifampicin/mg cells and M. tuberculosis had accumulated 154 ng rifampicin/mg cells. A steady-state concentration (SSC) of rifampicin was accumulated rapidly by M. aurum and M. tuberculosis within minutes of drug exposure, unlike M. smegmatis, which accumulated rifampicin more slowly. With an increase in the concentration of rifampicin from 0.12 mg/L to 2 mg/L there was an increase in the concentration of rifampicin accumulated by M. tuberculosis, with no detectable loss of viability over the 20 min of the accumulation experiment. With an increase in temperature there was also an increase in the concentration of rifampicin accumulated by M. tuberculosis; between 15 and 30 degrees C the increase was linear. For all three species sub-inhibitory concentrations of ethambutol increased the concentration of rifampicin accumulated. However, both growth and accumulation of rifampicin were lower in the presence of 0.05% Tween 80. Accumulation of rifampicin by M. smegmatis was unaffected by the presence of the proton motive force inhibitor, 2,4-dinitrophenol (1 mM), whether added before or after the addition of rifampicin to the mycobacterial culture. For all three species, the Gram-positive bacterial efflux inhibitor reserpine (20 mg/L) slightly increased the SSC of rifampicin, but the increase was not statistically significant. Addition of glucose to energize a putative efflux pump had little effect on the accumulation of rifampicin in the presence or absence of reserpine for M. tuberculosis; however, for M. aurum and M. smegmatis the reserpine effect was abolished by the addition of glucose. These data suggest that rifampicin may be removed from wild-type mycobacteria by efflux, but that the pump(s) is expressed at low level.