Stuertz K, Schmidt H, Eiffert H, Schwartz P, Mäder M, Nau R
Department of Neurology, University of Göttingen, Germany.
Antimicrob Agents Chemother. 1998 Feb;42(2):277-81. doi: 10.1128/AAC.42.2.277.
The release of lipoteichoic acid (LTA) and teichoic acid (TA) from a Streptococcus pneumoniae type 3 strain during exposure to ceftriaxone, meropenem, rifampin, rifabutin, quinupristin-dalfopristin, and trovafloxacin in tryptic soy broth was monitored by a newly developed enzyme-linked immunosorbent assay. At a concentration of 10 microg/ml, a rapid and intense release of LTA and TA occurred during exposure to ceftriaxone (3,248+/-1,688 ng/ml at 3 h and 3,827+/-2,133 ng/ml at 12 h) and meropenem (2,464+/-1,081 ng/ml at 3 h and 2,900+/-1,364 ng/ml at 12 h). Three hours after exposure to rifampin, rifabutin, quinupristin-dalfopristin, and trovafloxacin, mean LTA and TA concentrations of less than 460 ng/ml were observed (for each group, P < 0.01 versus the concentrations after exposure to ceftriaxone). After 12 h of treatment, the LTA and TA concentrations were 463+/-126 ng/ml after exposure to rifampin, 669+/-303 ng/ml after exposure to rifabutin, and 1,236+/-772 ng/ml after exposure to quinupristin-dalfopristin (for each group, P < 0.05 versus the concentrations after exposure to ceftriaxone) and 1,745+/-1,185 ng/ml after exposure to trovafloxacin (P = 0.12 versus the concentration after exposure to ceftriaxone). At 10 microg/ml, bactericidal antibacterial agents that do not primarily affect cell wall synthesis reduced the amount of LTA and TA released during their cidal action against S. pneumoniae in comparison with the amount released after exposure to beta-lactams. Larger quantities of LTA and TA were released after treatment with low concentrations (1x the MIC and 1x the minimum bactericidal concentration) than after no treatment for all antibacterial agents except the rifamycins. This does not support the concept of using a low first antibiotic dose to prevent the release of proinflammatory cell wall components.
采用新开发的酶联免疫吸附测定法,监测3型肺炎链球菌菌株在胰蛋白胨大豆肉汤中暴露于头孢曲松、美罗培南、利福平、利福布汀、奎奴普丁-达福普汀和曲伐沙星期间脂磷壁酸(LTA)和磷壁酸(TA)的释放情况。在浓度为10微克/毫升时,暴露于头孢曲松(3小时时为3248±1688纳克/毫升,12小时时为3827±2133纳克/毫升)和美罗培南(3小时时为2464±1081纳克/毫升,12小时时为2900±1364纳克/毫升)期间,LTA和TA迅速且大量释放。暴露于利福平、利福布汀、奎奴普丁-达福普汀和曲伐沙星3小时后,观察到LTA和TA的平均浓度低于460纳克/毫升(每组与暴露于头孢曲松后的浓度相比,P<0.01)。治疗12小时后,暴露于利福平后LTA和TA浓度为463±126纳克/毫升,暴露于利福布汀后为669±303纳克/毫升,暴露于奎奴普丁-达福普汀后为1236±772纳克/毫升(每组与暴露于头孢曲松后的浓度相比,P<0.05),暴露于曲伐沙星后为1745±一千一百八十五纳克/毫升(与暴露于头孢曲松后的浓度相比,P=0.12)。在10微克/毫升时,与暴露于β-内酰胺类药物后释放的量相比,主要不影响细胞壁合成的杀菌性抗菌药物在其对肺炎链球菌的杀菌作用期间减少了LTA和TA的释放量。除利福霉素外,所有抗菌药物在低浓度(1倍MIC和1倍最低杀菌浓度)治疗后释放的LTA和TA量均比未治疗时多。这并不支持使用低剂量初始抗生素来预防促炎细胞壁成分释放的概念。