Department of Microbiology, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.
Antimicrob Agents Chemother. 2013 Nov;57(11):5432-7. doi: 10.1128/AAC.01279-13. Epub 2013 Aug 19.
Gram-positive bacteria cause serious human illnesses through combinations of cell surface and secreted virulence factors. We initiated studies with four of these organisms to develop novel topical antibacterial agents that interfere with growth and exotoxin production, focusing on menaquinone analogs. Menadione, 1,4-naphthoquinone, and coenzymes Q1 to Q3 but not menaquinone, phylloquinone, or coenzyme Q10 inhibited the growth and to a greater extent exotoxin production of Staphylococcus aureus, Bacillus anthracis, Streptococcus pyogenes, and Streptococcus agalactiae at concentrations of 10 to 200 μg/ml. Coenzyme Q1 reduced the ability of S. aureus to cause toxic shock syndrome in a rabbit model, inhibited the growth of four Gram-negative bacteria, and synergized with another antimicrobial agent, glycerol monolaurate, to inhibit S. aureus growth. The staphylococcal two-component system SrrA/B was shown to be an antibacterial target of coenzyme Q1. We hypothesize that menaquinone analogs both induce toxic reactive oxygen species and affect bacterial plasma membranes and biosynthetic machinery to interfere with two-component systems, respiration, and macromolecular synthesis. These compounds represent a novel class of potential topical therapeutic agents.
革兰氏阳性菌通过细胞表面和分泌的毒力因子的组合引起严重的人类疾病。我们从这四种生物体开始研究,以开发新型局部抗菌剂,干扰生长和外毒素产生,重点是甲萘醌类似物。在浓度为 10 至 200 μg/ml 时,甲萘醌、1,4-萘醌和辅酶 Q1 至 Q3 但不是甲萘醌、叶绿醌或辅酶 Q10 抑制了金黄色葡萄球菌、炭疽芽孢杆菌、酿脓链球菌和无乳链球菌的生长,并在更大程度上抑制了外毒素的产生。辅酶 Q1 在兔模型中降低了金黄色葡萄球菌引起中毒性休克综合征的能力,抑制了四种革兰氏阴性菌的生长,并与另一种抗菌剂甘油单月桂酸酯协同抑制金黄色葡萄球菌的生长。已表明葡萄球菌双组分系统 SrrA/B 是辅酶 Q1 的抗菌靶标。我们假设甲萘醌类似物既诱导有毒的活性氧,又影响细菌的质膜和生物合成机制,从而干扰双组分系统、呼吸和大分子合成。这些化合物代表了一类新型潜在的局部治疗剂。