Proctor R A, Textor J A
Infect Immun. 1985 Aug;49(2):286-90. doi: 10.1128/iai.49.2.286-290.1985.
Recent work with lipid mutants of Escherichia coli and Salmonella typhimurium has helped to elucidate the correct structure of lipid A and has suggested a biosynthetic pathway. Precursor molecules include diacylglucosamine 1-phosphates and tetraacyl disaccharide bis-phosphates. The activities of several of these compounds and of their derivatives were measured by Limulus amebocyte lysate (LAL) assay. We report that (i) both mono- and disaccharide precursors of lipid A activate LAL, (ii) two acyl chains on the monosaccharide subunit of lipid A are necessary for activation of LAL, and (iii) the monosaccharide, 2-monoacylglucosamine 1-phosphate can competitively inhibit LAL activation by diacyl monosaccharide lipid A precursors. However, 2-monoacylglucosamine 1-phosphate did not inhibit endotoxin activation of LAL. One unanticipated finding was that the activities of the monosaccharides were reduced upon storage even though their covalent structures were unchanged. Perhaps this is due to alterations in physical state. Thus, these lipid A precursors and derivatives offer some insight into the structural features required for activation of the LAL assay and may in the future provide derivatives which are competitive inhibitors of endotoxin.
最近对大肠杆菌和鼠伤寒沙门氏菌脂质突变体的研究有助于阐明脂质A的正确结构,并提出了一条生物合成途径。前体分子包括二酰基葡糖胺1-磷酸酯和四酰基二糖双磷酸酯。通过鲎试剂(LAL)检测法测定了其中几种化合物及其衍生物的活性。我们报告:(i)脂质A的单糖和二糖前体均能激活LAL;(ii)脂质A单糖亚基上的两条酰基链是激活LAL所必需的;(iii)单糖2-单酰基葡糖胺1-磷酸酯能竞争性抑制二酰基单糖脂质A前体对LAL的激活。然而,2-单酰基葡糖胺1-磷酸酯并不抑制LAL的内毒素激活。一个意外发现是,即使单糖的共价结构未改变,其活性在储存后仍会降低。这可能是由于物理状态的改变。因此,这些脂质A前体和衍生物为LAL检测法激活所需的结构特征提供了一些见解,未来可能会提供作为内毒素竞争性抑制剂的衍生物。