Effect of lipid A-associated protein and lipid A on the expression of lipopolysaccharide activity. I. Immunological activity.
Effect of lipid A-associated protein and lipid A on the expression of lipopolysaccharide activity. I. Immunological activity.
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发表时间：
1980-07
期刊：
影响因子：
6.4
通讯作者：
S. Izui;D. Morrison;B. Curry;F. Dixon
中科院分区：
文献类型：
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作者：
S. Izui;D. Morrison;B. Curry;F. Dixon
详细研究了细菌内毒素的各种化学部分，即脂质A相关蛋白（Lipid A-associated protein，Lipid A）、脂质A和O-抗原多糖对这些活性细菌产物的许多免疫活性的贡献。利用了来自大肠杆菌0111：B4的抗原性相同的内毒素制剂的可用性，这些内毒素制剂的β-内酰胺和/或脂质A的含量差异很大。在小鼠脾细胞中启动体外增殖反应的能力在很大程度上与存在对脂质A的依赖性较弱（尽管仍然至关重要）的LPS有关。另一方面，体内多克隆抗体应答仅依赖于脂质A。在这方面，β-内酰胺酶的存在对非特异性低亲和力抗体的刺激没有明显影响。所有的制剂，无论脂质和脂质A的含量，刺激类似的体内增强抗体反应的蛋白抗原（佐剂）和特异性免疫反应的内毒素多糖抗原。结果强调了细菌内毒素制剂的体外B淋巴细胞增殖反应和体内免疫刺激反应之间缺乏相关性。这些数据还表明，脂质A对体内应答的贡献最小，而脂质A对佐剂活性和对O-抗原多糖的初次免疫应答的贡献极其有限。
A detailed investigation has been made of the contribution of the various chemical moieties of bacterial endotoxins, namely lipid A-associated protein (LAP), lipid A and O-antigen polysaccharide to a number of the immunological activities of these active bacterial products. Advantage was taken of the availability of antigenically identical endotoxin preparations from Escherichia coli 0111:B4 which differed greatly in their content of LAP and/or lipid A. The capacity to initiate in vitro proliferative responses in murine splenocytes was in a large part related to the presence of LAP with a less potent, although still critical, dependence upon lipid A. On the other hand, the in vivo polyclonal antibody response was dependent only upon lipid A. In this respect, the presence of LAP had no apparent effect on the stimulation of nonspecific low affinity antibody. All preparations, regardless of LAP and lipid A content, stimulated similar in vivo enhancement of antibody responses to a protein antigen (adjuvanticity) and specific immune responses to the endotoxin polysaccharide antigen. The results emphasize the lack of correlation between in vitro B lymphocyte proliferative responses and in vivo immunostimulatory responses of bacterial endotoxin preparations. These data also suggest a minimal contribution of LAP to in vivo responses and an extremely limited contribution of lipid A to the adjuvant activity and the primary immune response to O-antigen polysaccharide.