Wang Qun, Peng Bo, Song Mingyue, Li Jun, Miao Jianyin, Feng Konglong, Chen Feilong, Zhai Xiaoxiang, Cao Yong
College of Food Science, South China Agricultural University, Guangzhou, China.
Guangdong Haitian Innovation Technology Co., Ltd., Foshan, China.
Front Nutr. 2021 Nov 12;8:768890. doi: 10.3389/fnut.2021.768890. eCollection 2021.
Previous studies from our lab have shown that the antimicrobial peptide F1 obtained from the milk fermentation by FX-6 derived from Tibetan kefir was different from common antimicrobial peptides; specifically, F1 simultaneously inhibited the growth of Gram-negative and Gram-positive bacteria. Here, we present follow-on work demonstrating that after the antimicrobial peptide F1 acts on either ATCC 25922 () or ATCC 63589 (), their respective bacterial membranes were severely deformed. This deformation allowed leakage of potassium and magnesium ions from the bacterial membrane. The interaction between the antimicrobial peptide F1 and the bacterial membrane was further explored by artificially simulating the bacterial phospholipid membranes and then extracting them. The study results indicated that after the antimicrobial peptide F1 interacted with the bacterial membranes caused significant calcein leakage that had been simulated by different liposomes. Furthermore, transmission electron microscopy observations revealed that the phospholipid membrane structure was destroyed and the liposomes presented aggregation and precipitation. Quartz Crystal Microbalance with Dissipation (QCM-D) results showed that the antimicrobial peptide F1 significantly reduced the quality of liposome membrane and increased their viscoelasticity. Based on the study's findings, the phospholipid membrane particle size was significantly increased, indicating that the antimicrobial peptide F1 had a direct effect on the phospholipid membrane. Conclusively, the antimicrobial peptide F1 destroyed the membrane structure of both Gram-negative and Gram-positive bacteria by destroying the shared components of their respective phospholipid membranes which resulted in leakage of cell contents and subsequently cell death.
我们实验室之前的研究表明,从藏式开菲尔FX-6牛奶发酵中获得的抗菌肽F1与普通抗菌肽不同;具体而言,F1同时抑制革兰氏阴性菌和革兰氏阳性菌的生长。在此,我们展示后续工作,证明抗菌肽F1作用于ATCC 25922()或ATCC 63589()后,它们各自的细菌膜严重变形。这种变形使钾离子和镁离子从细菌膜泄漏。通过人工模拟细菌磷脂膜然后提取它们,进一步探索了抗菌肽F1与细菌膜之间的相互作用。研究结果表明,抗菌肽F1与不同脂质体模拟的细菌膜相互作用后导致钙黄绿素显著泄漏。此外,透射电子显微镜观察显示磷脂膜结构被破坏,脂质体出现聚集和沉淀。石英晶体微天平耗散(QCM-D)结果表明,抗菌肽F1显著降低了脂质体膜的质量并增加了其粘弹性。基于该研究的发现,磷脂膜粒径显著增加,表明抗菌肽F1对磷脂膜有直接影响。总之,抗菌肽F1通过破坏革兰氏阴性菌和革兰氏阳性菌各自磷脂膜的共同成分来破坏它们的膜结构,导致细胞内容物泄漏,随后细胞死亡。