Piatti G
Department of Pharmacology, School of Medicine, University of Milan, Italy.
Pharmacol Res. 1994 Dec;30(4):289-99. doi: 10.1016/1043-6618(94)80009-x.
Respiratory infections develop after contact and successive adhesion of micro-organisms to airway mucosa. In fact, the bacterial adhesins are able to interact with a 'lock and key' mechanism with the analogous structures on epithelial surfaces when permissive conditions occur. It was observed that antibiotics at subinhibitory concentrations (sub-MICs) can modify bacterial ability of adhesion to host cells, in various ways. Bacterial adhesion is generally inhibited by antibiotics that, at these concentrations, do not kill bacteria but can change the surface architecture of the micro-organisms.
呼吸道感染是在微生物接触并相继黏附于气道黏膜后发生的。事实上，当出现适宜条件时，细菌黏附素能够以“锁钥”机制与上皮表面的类似结构相互作用。据观察，亚抑菌浓度（亚 MIC）的抗生素能够以多种方式改变细菌对宿主细胞的黏附能力。在这些浓度下，抗生素一般不会杀死细菌，但可改变微生物的表面结构，从而抑制细菌黏附。
