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克拉霉素的亚致死浓度会干扰金黄色葡萄球菌对人细胞的黏附性表达。

Sub-lethal concentrations of clarithromycin interfere with the expression of Staphylococcus aureus adhesiveness to human cells.

作者信息

Braga P C, Piatti G

机构信息

Center for Respiratory Pharmacology, School of Medicine, University of Milan, Italy.

出版信息

J Chemother. 1993 Jun;5(3):159-63. doi: 10.1080/1120009x.1993.11739226.

DOI:10.1080/1120009x.1993.11739226
PMID:8371124
Abstract

It has been known for some time that some antibiotics, generally at sub-lethal concentrations, are able to alter the morphology and the shape of bacteria. However, more subtle molecular alterations can also be present, such as disorganization of bacterial surface architecture, which leads to changes in the surface electrical charge that can influence the forces of attraction or repulsion responsible for interaction of bacterial surfaces with environmental surfaces. Bacterial adhesion to epithelial cells is a phenomenon regulated by these mechanisms. Clarithromycin, a new macrolide, at sub-inhibitory concentrations from 1/2 to 1/16 of the MIC, that is to say, from 0.12 to 0.015 microgram/ml, significantly reduces adhesion of Staphylococcus aureus to human buccal epithelial cells. Clarithromycin, as other antibiotics that interfere with the bacterial protein synthesis, should also be able to disturb the synthesis of adhesins. These are ligand molecules located on the surface of bacteria, and thus reduce the ability of bacteria to bind specifically to complementary molecules on the surfaces of epithelial cells which is necessary for host colonization.

摘要

一段时间以来,人们已经知道某些抗生素通常在亚致死浓度下能够改变细菌的形态和形状。然而,也可能存在更细微的分子改变,例如细菌表面结构的紊乱,这会导致表面电荷的变化,进而影响负责细菌表面与环境表面相互作用的吸引力或排斥力。细菌对上皮细胞的黏附是受这些机制调节的一种现象。克拉霉素是一种新型大环内酯类抗生素,在亚抑制浓度(即MIC的1/2至1/16,也就是0.12至0.015微克/毫升)下,能显著降低金黄色葡萄球菌对人颊上皮细胞的黏附。与其他干扰细菌蛋白质合成的抗生素一样,克拉霉素也应该能够干扰黏附素的合成。黏附素是位于细菌表面的配体分子,因此会降低细菌与上皮细胞表面互补分子特异性结合的能力,而这种结合对于宿主定植是必需的。

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