莫西沙星对人外周血单个核细胞促炎细胞因子产生的影响。
Effect of moxifloxacin on production of proinflammatory cytokines from human peripheral blood mononuclear cells.
作者信息
Choi Jung-Hyun, Song Min-Jin, Kim Seung-Han, Choi Su-Mi, Lee Dong-Gun, Yoo Jin-Hong, Shin Wan-Shik
机构信息
Division of Infectious Disease, Department of Internal Medicine, College of Medicine, Catholic University of Korea, Seoul, Korea.
出版信息
Antimicrob Agents Chemother. 2003 Dec;47(12):3704-7. doi: 10.1128/AAC.47.12.3704-3707.2003.
Abstract
The effects of moxifloxacin, a new methoxyfluoroquinolone, on the production of proinflammatory cytokines from human peripheral blood mononuclear cells (PBMCs) were evaluated. Moxifloxacin inhibited the production of tumor necrosis factor alpha (TNF-alpha) and/or interleukin-6 (IL-6) by PBMCs stimulated with lipopolysaccharide (LPS), lipoteichoic acid (LTA), and heat-killed bacteria in a concentration-dependent manner without cytotoxic effects. The addition of moxifloxacin reduced the population of cells positive for CD-14 and TNF-alpha and for CD-14 and IL-6 among the LPS- or LTA-stimulated PBMCs. By Western blot analysis, moxifloxacin pretreatment reduced the degradation of IkappaBalpha in LPS-stimulated PBMCs. In conclusion, moxifloxacin could interfere with NF-kappaB activation by inhibiting the degradation of IkappaBalpha and reduce the levels of production of proinflammatory cytokines.
摘要
评估了新型甲氧基氟喹诺酮莫西沙星对人外周血单个核细胞（PBMC）促炎细胞因子产生的影响。莫西沙星以浓度依赖的方式抑制脂多糖（LPS）、脂磷壁酸（LTA）和热灭活细菌刺激的PBMC产生肿瘤坏死因子α（TNF-α）和/或白细胞介素-6（IL-6），且无细胞毒性作用。添加莫西沙星可减少LPS或LTA刺激的PBMC中CD-14和TNF-α双阳性以及CD-14和IL-6双阳性细胞的数量。通过蛋白质免疫印迹分析，莫西沙星预处理可减少LPS刺激的PBMC中IkappaBalpha的降解。总之，莫西沙星可通过抑制IkappaBalpha的降解干扰核因子κB（NF-κB）的激活，并降低促炎细胞因子的产生水平。
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