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Antibacterial activity and mechanism of bifidocin A against Listeria monocytogenes

机译:双歧孔A对李斯特菌单核细胞增生的抗菌活性及机制

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Bifidocin A, produced by Bifidobacterium animalis BB04, is a novel bacteriocin with antimicrobial activity against a wide range of gram-positive and gram-negative foodborne bacteria. The objective of this study was to investigate the antibacterial activity and mechanism of action of bifidocin A against Listeria monocytogenes, one of the most susceptible bacteria to this bacteriocin. The minimum inhibitory concentration (MIC) of bifidocin A for L monocytogenes 35152 was 0.029 mg/mL. Time-kill assays showed that bifidocin A effectively inhibited the growth of L monocytogenes in a time-and concentration dependent manner. The mechanism of action of bifidocin A was studied by analyzing its effects at a MIC on the cell morphology, intracellular organization, membrane permeability, membrane integrity, and membrane proton motive force (PMF) of L monocytogenes. Scanning and transmission electron microscopy analyses showed that bifidocin A induced alterations in the morphology and intracellular organization of L monocytogenes cells. Confocal laser scanning microscopy images showed that L monocytogenes cells treated with bifidocin A took up propidium iodide. Bifidocin A treatment also induced the leakage of K+ and inorganic phosphate, the hydrolysis and release of ATP, and a collapse of the transmembrane electrical potential and pH gradient in L. monocytogenes cells. These results suggested that bifidocin A exerted its anti-Listeria monocytogenes effect through the dissipation of the cytoplasmic membrane PMF, increased membrane permeability, cell membrane pore formation, destruction of membrane integrity, and ultimately complete disintegration of the cells. (C) 2016 Elsevier Ltd. All rights reserved.
机译:由双歧杆菌BB04产生的双歧膜A,是一种新的伯霉素,其具有针对各种革兰氏阳性和革兰氏阴性食物染额细菌的抗微生物活性。本研究的目的是研究双歧膜A对李斯特菌单核细胞增生的抗菌活性和作用机制,这是这种细菌的最敏感的细菌之一。 L单核细胞增生35152的双离析蛋白A的最小抑制浓度(MIC)为0.029mg / ml。时间杀死测定表明,双离心蛋白A有效地抑制了一种时间和浓度依赖性方式的L单核细胞增生的生长。通过分析其在MIC上的细胞形态,细胞内组织,膜渗透性,膜完整性和L单核细胞增生的膜质子动力(PMF)的效果来研究双歧膜蛋白A的作用机制。扫描和透射电子显微镜分析表明,双离析蛋白是L单核细胞元细胞的形态和细胞内组织中的诱导的改变。共聚焦激光扫描显微镜图像显示用双歧孔A处理的单核细胞元细胞占用碘化丙啶。双离析蛋白治疗还诱导了K +和无机磷酸盐的泄漏,ATP的水解和释放,以及L.单核细胞增生细胞中的跨膜电势和pH梯度的塌陷。这些结果表明,双歧膜通过耗散细胞质膜PMF,增加膜渗透性,细胞膜孔形成,膜完整性的破坏以及最终完全崩解细胞的抗李斯特菌单核细胞增生。 (c)2016 Elsevier Ltd.保留所有权利。

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