Proctor R A
Infect Immun. 1979 Sep;25(3):912-21. doi: 10.1128/iai.25.3.912-921.1979.
Endotoxin was shown to depress neutrophil bactericidal activity while enhancing Nitro Blue Tetrazolium reduction and hexose monophosphate shunt activity. Separation of bactericidal action from oxidative metabolism suggests that the effect of endotoxin might involve the formation of reactive oxygen radicals such as superoxide. Chemiluminescence often accompanies metabolic activation of polymorphonuclear neutrophils (PMNs). However, human PMNs did not show chemiluminescence when challenged with endotoxin (lipopolysaccharide; LPS) or lipid A. Superoxide formation was also unaffected by endotoxin. In contrast, preincubation of PMNs with LPS for 30 min produced significant depression of chemiluminescence, oxygen consumption, and superoxide formation. Decreased chemiluminescence was not the result of complement consumption. In a cell-free system, superoxide was not scavenged by LPS, nor did LPS stimulate superoxide dismutase. Oxidase enzymes for reduced nicotinamide adenine dinucleotide or reduced nicotinamide adenine dinucleotide phosphate harvested from broken cells were not affected by LPS. The toxicity of LPS may reside in its ability to activate the PMNs while simultaneously blocking bactericidal capacity.
内毒素可抑制中性粒细胞的杀菌活性，同时增强硝基蓝四唑还原作用和磷酸己糖旁路活性。杀菌作用与氧化代谢的分离表明，内毒素的作用可能涉及超氧阴离子等活性氧自由基的形成。化学发光常伴随多形核中性粒细胞（PMNs）的代谢激活。然而，人PMNs在用内毒素（脂多糖；LPS）或脂质A刺激时未表现出化学发光。超氧阴离子的形成也不受内毒素影响。相反，将PMNs与LPS预孵育30分钟会导致化学发光、氧消耗和超氧阴离子形成显著降低。化学发光降低并非补体消耗的结果。在无细胞系统中，LPS不会清除超氧阴离子，也不会刺激超氧化物歧化酶。从破碎细胞中获取的还原型烟酰胺腺嘌呤二核苷酸或还原型烟酰胺腺嘌呤二核苷酸磷酸的氧化酶不受LPS影响。LPS的毒性可能在于其激活PMNs的同时阻断杀菌能力。
