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首页> 外文期刊>Journal of endotoxin research >Lipid-mediated resistance of Gram-negative bacteria against various pore-forming antimicrobial peptides.
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Lipid-mediated resistance of Gram-negative bacteria against various pore-forming antimicrobial peptides.

机译：脂质介导的革兰氏阴性细菌对各种成孔抗菌肽的抗性。

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摘要

Lipopolysaccharides (LPSs) play a dual role as target and as effector molecules. The knowledge of the LPS-induced activation of human immune cells is increasing; however, surprisingly, much less effort seems to be directed towards the understanding of the mechanisms leading to the killing of the bacterial organisms, which eventually results in the release of LPS from the bacterial surface into the blood circulation. We demonstrate mechanisms of interaction of peptides of the innate immune system (e.g. defensins and cathelicidins) as well as of externally administered antibiotics (e.g. Polymyxin B) with Gram-negative bacteria. The main focus is directed on data derived from electrical measurements on a reconstitution system of the outer membrane as an asymmetric bilayer composed on one side of LPS and on the other of phospholipids. All these antimicrobial peptides (AMPs) are membrane-active and induce the permeabilization of the reconstituted membranes by the formation of lesions. We found that differences in the activity of the AMPs against various sensitive and resistant Gram-negative bacteria can be explained solely by variations in the chemical structure of LPS, e.g. in the composition of the sugar head group. A reduction of the net negative charge of LPS is responsible for a reduced interaction with the polycationic AMPs and thus for resistance. A most important side effect of positively charged AMPs is the neutralization of the negatively charged LPS released from the bacterial surface as a consequence of AMP-induced killing.
机译：脂多糖（LPS）担当靶标和效应分子的双重角色。 LPS诱导的人类免疫细胞激活的知识正在增加。然而，令人惊讶的是，似乎要花费更少的精力来理解导致细菌生物杀灭的机制，这最终导致LPS从细菌表面释放到血液循环中。我们证明了先天免疫系统（例如防御素和cathelicidins）以及外部施用的抗生素（例如多粘菌素B）与革兰氏阴性细菌的肽相互作用的机制。主要关注点是针对在LPS的一侧和磷脂的另一侧组成的不对称双层外膜重构系统的电学测量数据。所有这些抗菌肽（AMPs）具有膜活性，并通过损伤的形成诱导重构膜的通透性。我们发现，AMP对各种敏感和抗性革兰氏阴性细菌的活性差异可以仅通过LPS的化学结构变化来解释，例如LPS。在糖头组的组成。 LPS净负电荷的减少是与聚阳离子AMPs相互作用减少的原因，因此也是电阻的原因。带正电的AMPs最重要的副作用是中和从细菌表面释放的带负电的LPS，这是AMP诱导的杀伤的结果。

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