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首页> 外文期刊>Biochemistry >Lipopolysaccharides in Bacterial Membranes Act like Cholesterol in Eukaryotic Plasma Membranes in Providing Protection against Melittin-Induced Bilayer Lysis
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Lipopolysaccharides in Bacterial Membranes Act like Cholesterol in Eukaryotic Plasma Membranes in Providing Protection against Melittin-Induced Bilayer Lysis

机译：细菌膜中的脂多糖的作用类似于真核生物血浆膜中的胆固醇，可提供针对蜂毒毒素诱导的双层裂解的保护作用。

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Melittin is a small, cationic peptide that, like many other antimicrobial peptides, lyses cell membranes by acting on their lipid bilayers. However, the sensitivity to antimicrobial peptides varies among cell types. We have performed direct binding and vesicle leakage experiments to determine the sensitivity to melitin of bilayers composed of various physiologically relevant lipids, in particular, key components of eukaryotic membranes (cholesterol) and bacterial outer membranes (lipopolysaccharide or LPS). Melittin binds to bilayers composed of both zwiterionic and negatively charged phospholipids, as well as to the highly charged LPS bilayers. The magnitude of the free energy of binding (DELTAG~°) increases with increasing bilayer charge density: DELTAG = - 7.6 kcal/mol for phosphatidylcholine (PC) bilayer and - 8.9 to -11.0 kcal/mol for negatively charged bilayers containing phosphatidylserine (PS), phospholipids with covalently attached polyethylene glycol (PEG-lipids), or LPS. Comparisons of these data show that binding is not markedly affected by the steric barrier produced by the PEG in PEG-lipids or by the polysaccharide core of LPS. The addition of equimolar cholesterol to PC bilayers reduces the level of binding (DELTAG~°= 6.4 kcal/mol) and reduces the extent of melittin-induced leakage by 20-fold. LPS and 1:1 PC/cholesterol bilayers have similar high resistance to melittin-induced leakage, indicating that cholesterol in eukaryotic plasma membranes and LPS in Gram-negative bacteria provide strong protection against the lytic effects of melittin. We argue that this resistance is due at least in part to the similar tight packaging of the lipid acyl chains in PC/cholesterol and LPS bilayers. The addition of bacterial phospholipids to LPS bilayers increases ther sensitivity to melittin, helping to explain the higher sensitivity of deep rough bacteria compared ot smooth phenotypes.
机译：蜂毒肽是一种小的阳离子肽，与许多其他抗菌肽一样，它通过作用于它们的脂质双层来裂解细胞膜。但是，对抗菌肽的敏感性随细胞类型而变化。我们已经进行了直接结合和囊泡渗漏实验，以确定由各种生理相关脂质，尤其是真核膜（胆固醇）和细菌外膜（脂多糖或LPS）的关键成分组成的双层对蜂毒蛋白的敏感性。蜂毒肽结合由两性离子和带负电的磷脂组成的双层，以及与高电荷的LPS双层结合。结合自由能的大小（DELTAG〜°）随着双层电荷密度的增加而增加：DELTAG =-磷脂酰胆碱（PC）双层的7.6 kcal / mol和-含磷脂酰丝氨酸（PS）的带负电荷的双层的-8.9至-11.0 kcal / mol ），磷脂与共价连接的聚乙二醇（PEG-脂质）或LPS。这些数据的比较表明，结合不受PEG在PEG脂质中或LPS多糖核心产生的空间屏障的影响。向PC双层中添加等摩尔胆固醇可降低结合水平（DELTAG〜°= 6.4 kcal / mol），并将蜂毒素引起的渗漏程度降低20倍。 LPS和1：1 PC /胆固醇双层膜对蜂毒肽诱导的渗漏具有相似的高抗性，表明真核生物质膜中的胆固醇和革兰氏阴性细菌中的LPS为抵抗蜂毒肽的溶解作用提供了强有力的保护。我们认为这种抗药性至少部分是由于PC /胆固醇和LPS双层中脂质酰基链的紧密包装所致。向LPS双层膜中添加细菌磷脂可提高其对蜂毒蛋白的敏感性，从而有助于解释与光滑表型相比，深层粗糙细菌的敏感性更高。

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