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[四环素类抗生素的细菌耐药机制]

[Bacterial resistance mechanisms for tetracyclines].

作者信息

Yamaguchi A

机构信息

Institute of Scientific and Industrial Research, Osaka University.

出版信息

Nihon Rinsho. 1997 May;55(5):1245-51.

PMID:9155182
Abstract

Tetracycline resistance mechanism is unique in bacterial resistance mechanisms because of being mainly based on the drug efflux except for the ribosomal protection mechanism in some tetracycline-resistant Gram-positive bacteria. Tetracycline efflux proteins such as Tet(B) and Tet(C) of Gram-negative bacteria are estimated to have 12-membrane-spanning structure common to the major facilitator family transporters. We experimentally proved the 12-membrane-spanning structure of Tet(B) by site-directed chemical labeling. On the other hand, the tetracycline efflux proteins such as Tet(K) and Tet(L) of Gram-positive bacteria are estimated to have 14-membrane-spanning structure. We first presented the experimental evidence for the 14-spanning structure of Tet(K) based on the Tet(K)-PhoA fusion protein analysis. Another mechanism of tetracycline resistance is a ribosomal protection encoded by tet(M) and let(O). These genes encode the elongation factor(EF-Tu or EF-G)-like protein, whereas the molecular mechanism of the resistance has not yet been revealed.

摘要

四环素耐药机制在细菌耐药机制中是独特的,因为除了一些耐四环素革兰氏阳性菌中的核糖体保护机制外,其主要基于药物外排。革兰氏阴性菌的四环素外排蛋白,如Tet(B)和Tet(C),据估计具有主要转运体家族转运蛋白共有的12次跨膜结构。我们通过定点化学标记实验证明了Tet(B)的12次跨膜结构。另一方面,革兰氏阳性菌的四环素外排蛋白,如Tet(K)和Tet(L),据估计具有14次跨膜结构。我们首次基于Tet(K)-PhoA融合蛋白分析给出了Tet(K)的14次跨膜结构的实验证据。四环素耐药的另一种机制是由tet(M)和let(O)编码的核糖体保护。这些基因编码延伸因子(EF-Tu或EF-G)样蛋白,但其耐药的分子机制尚未阐明。

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