鼠李糖脂,糖脂生物表面活性剂的主要类别,由于它们作为针对多种病原菌的有效抗菌剂的相关性,最近在医学领域获得了极大的关注。我们以前的研究表明,来自铜绿假单胞菌UKMP14T环境分离株的鼠李糖脂具有抗菌作用,抗多药耐药ESKAPE(屎肠球菌,金黄色葡萄球菌,肺炎克雷伯菌,鲍曼不动杆菌,铜绿假单胞菌和肠杆菌。)病原体。然而,其抗菌作用机制尚不清楚。因此,本研究旨在通过研究一种ESKAPE病原体的细胞变化来阐明铜绿假单胞菌UKMP14T鼠李糖脂的抗菌作用机制,鲍曼不动杆菌,这是最难杀死的菌株。结果显示,如通过接触角测量所评估的,鼠李糖脂处理使鲍曼不动杆菌细胞更具疏水性。在鼠李糖脂浓度为1000μg/mL时,它还诱导释放510μg/mL的细胞蛋白质。此外,鼠李糖脂被发现具有杀菌作用,因为它们可以渗透内膜,导致核苷酸泄漏.如通过荧光显微镜观察到的,发现超过50%的细胞在1000μg/mL鼠李糖脂处理后被杀死。其他细胞变化,如不规则的形状和大小,膜扰动,结块,收缩和物理损伤在扫描电镜中清晰可见,FESEM和激光显微照片。此外,鼠李糖脂治疗抑制了鲍曼不动杆菌中酰基高丝氨酸内酯(AHLs)的水平,这对它们的生物膜形成和毒力至关重要。获得的结果表明,铜绿假单胞菌UKMP14T鼠李糖脂通过渗透靶向细菌外膜和内膜,包括对细胞的物理损伤,导致细胞泄漏。此外,AHL抑制似乎是它们的抗生物膜作用背后的机制。所有这些观察结果都与鼠李糖脂对鲍曼不动杆菌的抗菌作用有关。
Rhamnolipids, a major category of glycolipid biosurfactant, have recently gained enormous attention in medical field because of their relevance as effective antibacterial agents against a wide variety of pathogenic bacteria. Our previous studies have shown that
rhamnolipids from an environmental isolate of Pseudomonas aeruginosa UKMP14T possess antibacterial, anti-adhesive and anti-biofilm activity against multidrug-resistant ESKAPE (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and Enterobacter sp.) pathogens. However, the mechanism of their antibacterial action remains unclear. Thus, this study aimed to elucidate the mechanism of the antibacterial action of P. aeruginosa UKMP14T rhamnolipids by studying the changes in cells of one of the ESKAPE pathogens, Acinetobacter baumannii, which is the most difficult strain to kill. Results revealed that rhamnolipid treatment rendered A. baumannii cells more hydrophobic as evaluated through contact angle measurements. It also induced the release of cellular proteins measuring 510 μg/mL at a rhamnolipid concentration of 1000 μg/mL. In addition,
rhamnolipids were found to be bactericidal in their action as they could permeate the inner membranes, leading to a leak-out of nucleotides. More than 50 % of the cells were found to be killed upon 1000 μg/mL rhamnolipid treatment as observed through fluorescence microscopy. Other cellular changes such as irregular shape and size, membrane perturbations, clumping, shrinkage and physical damage were clearly visible in SEM, FESEM and laser micrographs. Furthermore, rhamnolipid treatment inhibited the levels of acyl-homoserine lactones (AHLs) in A. baumannii, which are vital for their biofilm formation and virulence. The obtained results indicate that P. aeruginosa UKMP14T
rhamnolipids target outer and inner bacterial membranes through permeation, including physical damage to the cells, leading to cell leakage. Furthermore, AHL inhibition appears to be the mechanism behind their anti-biofilm action. All these observations can be correlated to
rhamnolipids\' antibacterial effect against A. baumannii.