Ouberai Myriam, El Garch Farid, Bussiere Antoine, Riou Mickael, Alsteens David, Lins Laurence, Baussanne Isabelle, Dufrêne Yves F, Brasseur Robert, Decout Jean-Luc, Mingeot-Leclercq Marie-Paule
Université catholique de Louvain, Louvain Drug Research Institute, Unité de Pharmacologie Cellulaire et Moléculaire, UCL 73.70, avenue E. Mounier 73, B-1200 Bruxelles, Belgium.
Biochim Biophys Acta. 2011 Jun;1808(6):1716-27. doi: 10.1016/j.bbamem.2011.01.014. Epub 2011 Feb 1.
Aminoglycosides are among the most potent antimicrobials to eradicate Pseudomonas aeruginosa. However, the emergence of resistance has clearly led to a shortage of treatment options, especially for critically ill patients. In the search for new antibiotics, we have synthesized derivatives of the small aminoglycoside, neamine. The amphiphilic aminoglycoside 3',4',6-tri-2-naphtylmethylene neamine (3',4',6-tri-2NM neamine) has appeared to be active against sensitive and resistant P. aeruginosa strains as well as Staphylococcus aureus strains (Baussanne et al., 2010). To understand the molecular mechanism involved, we determined the ability of 3',4',6-tri-2NM neamine to alter the protein synthesis and to interact with the bacterial membranes of P. aeruginosa or models mimicking these membranes. Using atomic force microscopy, we observed a decrease of P. aeruginosa cell thickness. In models of bacterial lipid membranes, we showed a lipid membrane permeabilization in agreement with the deep insertion of 3',4',6-tri-2NM neamine within lipid bilayer as predicted by modeling. This new amphiphilic aminoglycoside bound to lipopolysaccharides and induced P. aeruginosa membrane depolarization. All these effects were compared to those obtained with neamine, the disubstituted neamine derivative (3',6-di-2NM neamine), conventional aminoglycosides (neomycin B and gentamicin) as well as to compounds acting on lipid bilayers like colistin and chlorhexidine. All together, the data showed that naphthylmethyl neamine derivatives target the membrane of P. aeruginosa. This should offer promising prospects in the search for new antibacterials against drug- or biocide-resistant strains.
氨基糖苷类药物是根除铜绿假单胞菌最有效的抗菌药物之一。然而,耐药性的出现显然导致了治疗选择的短缺,尤其是对重症患者而言。在寻找新型抗生素的过程中,我们合成了小氨基糖苷类新霉素的衍生物。两亲性氨基糖苷3',4',6 - 三 - 2 - 萘基亚甲基新霉素(3',4',6 - 三 - 2NM新霉素)似乎对敏感和耐药的铜绿假单胞菌菌株以及金黄色葡萄球菌菌株均具有活性(博桑内等人,2010年)。为了解其中涉及的分子机制,我们测定了3',4',6 - 三 - 2NM新霉素改变蛋白质合成以及与铜绿假单胞菌细胞膜或模拟这些细胞膜的模型相互作用的能力。使用原子力显微镜,我们观察到铜绿假单胞菌细胞厚度减小。在细菌脂质膜模型中,我们发现脂质膜通透性增加,这与建模预测的3',4',6 - 三 - 2NM新霉素在脂质双层中的深度插入一致。这种新型两亲性氨基糖苷与脂多糖结合并诱导铜绿假单胞菌细胞膜去极化。所有这些效应均与新霉素、二取代新霉素衍生物(3',6 - 二 - 2NM新霉素)、传统氨基糖苷类药物(新霉素B和庆大霉素)以及作用于脂质双层的化合物(如多粘菌素和氯己定)所产生的效应进行了比较。总体而言,数据表明萘基甲基新霉素衍生物靶向铜绿假单胞菌的细胞膜。这在寻找针对耐药菌株的新型抗菌药物方面应具有广阔的前景。