Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Department of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL 33620, USA.
Cell Chem Biol. 2019 Oct 17;26(10):1355-1364.e4. doi: 10.1016/j.chembiol.2019.07.009. Epub 2019 Aug 8.
Aminoglycoside antibiotics require proton motive force (PMF) for bacterial internalization. In non-respiring populations, PMF drops below the level required for drug influx, limiting the utility of aminoglycosides against strict and facultative anaerobes. We recently demonstrated that rhamnolipids (RLs), biosurfactant molecules produced by Pseudomonas aeruginosa, potentiate aminoglycoside activity against Staphylococcus aureus. Here, we demonstrate that RLs induce PMF-independent aminoglycoside uptake to restore sensitivity to otherwise tolerant persister, biofilm, small colony variant, and anaerobic populations of S. aureus. Furthermore, we show that this approach represses the rise of resistance, restores sensitivity to highly resistant clinical isolates, and is effective against other Gram-positive pathogens. Finally, while other membrane-acting agents can synergize with aminoglycosides, induction of PMF-independent uptake is uncommon, and distinct to RLs among several compounds tested. In all, small-molecule induction of PMF-independent aminoglycoside uptake circumvents phenotypic tolerance, overcomes genotypic resistance, and expands the utility of aminoglycosides against intrinsically recalcitrant bacterial populations.
氨基糖苷类抗生素需要质子动力势 (PMF) 才能进入细菌内部。在非呼吸群体中,PMF 下降到药物流入所需的水平以下,限制了氨基糖苷类药物对严格厌氧菌和兼性厌氧菌的效用。我们最近证明,铜绿假单胞菌产生的生物表面活性剂鼠李糖脂 (RL) 可以增强氨基糖苷类药物对金黄色葡萄球菌的活性。在这里,我们证明 RLs 诱导 PMF 不依赖的氨基糖苷摄取,以恢复对其他耐受的持续存在、生物膜、小菌落变体和金黄色葡萄球菌厌氧群体的敏感性。此外,我们表明这种方法抑制了耐药性的上升,恢复了对高度耐药的临床分离株的敏感性,并且对其他革兰氏阳性病原体有效。最后,虽然其他膜作用剂可以与氨基糖苷类药物协同作用,但 PMF 不依赖摄取的诱导并不常见,而且在几种测试的化合物中,RLs 是独特的。总之,小分子诱导 PMF 不依赖的氨基糖苷摄取可以规避表型耐受性,克服基因型耐药性,并扩大氨基糖苷类药物对固有难治性细菌群体的应用。