Anti-Biofilm Effects of Synthetic Antimicrobial Peptides Against Drug-Resistant Pseudomonas aeruginosa and Staphylococcus aureus Planktonic Cells and Biofilm
Anti-Biofilm Effects of Synthetic Antimicrobial Peptides Against Drug-Resistant Pseudomonas aeruginosa and Staphylococcus aureus Planktonic Cells and Biofilm
复制标题
DOI：
10.3390/molecules24244560
复制
发表时间：
2019-12-01
期刊：
影响因子：
4.6
通讯作者：
Jang, Mi-Kyeong
中科院分区：
文献类型：
--
作者：
Park, Seong-Cheol;Lee, Min-Young;Jang, Mi-Kyeong
生物膜相关感染难以管理或治疗，因为生物膜或嵌入生物膜的细菌难以根除。抗菌肽通过破坏细胞质膜来抑制浮游细菌的生长，因此作为对抗耐药微生物的一种可能的替代药物而受到越来越多的关注。本研究研究了合成肽（PS1-2、PS1-5和PS1-6）和常规抗生素对耐药铜绿假单胞菌和金黄色葡萄球菌生长、生物膜形成和生物膜还原的影响。PS1-2、PS1-5和PS1-6的作用也通过小鼠模型在体内进行了测试。所有肽均以剂量依赖的方式抑制浮游细胞生长和生物膜的形成。他们还通过去除碳水化合物、细胞外DNA和构成细胞外聚合物质（eps）但不影响蛋白质的脂质来减少预形成的生物膜团块。在体内，PS1-2对预成型生物膜表现出最大的抑制作用，且无细胞毒性。我们的研究结果表明，PS1-2肽具有作为下一代治疗药物克服多药耐药和调节生物膜相关感染的炎症反应的潜力。
Biofilm-associated infections are difficult to manage or treat as biofilms or biofilm-embedded bacteria are difficult to eradicate. Antimicrobial peptides have gained increasing attention as a possible alternative to conventional drugs to combat drug-resistant microorganisms because they inhibit the growth of planktonic bacteria by disrupting the cytoplasmic membrane. The current study investigated the effects of synthetic peptides (PS1-2, PS1-5, and PS1-6) and conventional antibiotics on the growth, biofilm formation, and biofilm reduction of drug-resistant Pseudomonas aeruginosa and Staphylococcus aureus. The effects of PS1-2, PS1-5, and PS1-6 were also tested in vivo using a mouse model. All peptides inhibited planktonic cell growth and biofilm formation in a dose-dependent manner. They also reduced preformed biofilm masses by removing the carbohydrates, extracellular DNA, and lipids that comprised extracellular polymeric substances (EPSs) but did not affect proteins. In vivo, PS1-2 showed the greatest efficacy against preformed biofilms with no cytotoxicity. Our findings indicate that the PS1-2 peptide has potential as a next-generation therapeutic drug to overcome multidrug resistance and to regulate inflammatory response in biofilm-associated infections.