Said A A, Livermore D M, Williams R J
Department of Medical Microbiology, London Hospital Medical College.
J Med Microbiol. 1987 Nov;24(3):267-74. doi: 10.1099/00222615-24-3-267.
During growth in magnesium (Mg++)-deficient mineral media, Pseudomonas aeruginosa cells synthesise large amounts of H1 outer-membrane protein and are resistant to polymyxins and EDTA. It has been suggested that H1 protein replaces Mg++ as an outer-membrane-stabilising component in Mg++-deprived cells, thereby removing the EDTA target and blocking an adsorption site for polymyxins. Induction of H1 protein synthesis also occurred in P. aeruginosa cells grown in Antibiotic No. 3 Broth (Ab3B), although this medium is not Mg++-deficient. Generally, significant induction of H1 protein did not occur in P. aeruginosa cultures grown in other complex media such as Proteose Peptone and Nutrient Broth, which contained less Mg++ than Ab3B, nor in Isosensitest Broth or Mueller Hinton Broth, which contained higher Mg++ concentrations. H1-protein-induced P. aeruginosa cells from Ab3B cultures, unlike those from Mg++-deficient mineral-broth culture, remained fully sensitive to polymyxin B and, with one exception, to EDTA. It is concluded that induction of H1 protein does not itself confer resistance to polymyxin B, and has no more than a minor role in EDTA resistance. Other cell-wall changes, such as phospholipid modifications and the absence of Mg++, probably account for the resistance of Mg++-deprived cells.
在缺镁(Mg++)的矿物培养基中生长时,铜绿假单胞菌细胞会合成大量的H1外膜蛋白,并且对多粘菌素和EDTA具有抗性。有人提出,在缺乏Mg++的细胞中,H1蛋白取代Mg++作为外膜稳定成分,从而消除了EDTA的作用靶点并阻断了多粘菌素的吸附位点。在3号抗生素肉汤(Ab3B)中生长的铜绿假单胞菌细胞中也会诱导H1蛋白的合成,尽管这种培养基并不缺镁。一般来说,在其他复杂培养基(如蛋白胨肉汤和营养肉汤,其Mg++含量低于Ab3B)中生长的铜绿假单胞菌培养物,以及在Mg++浓度较高的等敏感肉汤或穆勒-欣顿肉汤中生长的培养物,均未出现H1蛋白的显著诱导。与来自缺镁矿物肉汤培养物的细胞不同,来自Ab3B培养物的H1蛋白诱导的铜绿假单胞菌细胞对多粘菌素B仍完全敏感,并且除了一个例外,对EDTA也敏感。得出的结论是,H1蛋白的诱导本身并不会赋予对多粘菌素B的抗性,并且在EDTA抗性中只起次要作用。其他细胞壁变化,如磷脂修饰和Mg++的缺乏,可能是缺乏Mg++的细胞产生抗性的原因。