Takenaka A, Nakamura T, Mori R, Shibasaki H, Kondo S, Hisatsune K
J Neurol Sci. 1982 Aug;55(2):165-74. doi: 10.1016/0022-510x(82)90098-3.
Bacterial lipopolysaccharide (LPS)-induced protection against experimental allergic encephalomyelitis (EAE) was studied in guinea pigs using chemically modified derivatives. Hydroxylaminolysis or alkaline hydrolysis of LPS, by which ester-linked fatty acids are removed from LPS, resulted in total loss of its mitogenic activity for B lymphocytes, and EAE-suppressive activity was simultaneously reduced. Similar diminished activity was observed in delayed-type skin reactions to myelin basic protein (BP) and anti-BP antibody production detected by passive hemagglutination and enzyme-linked immunosorbent assay (ELISA). These results indicate that the active site of LPS in suppressing EAE is in the lipid portion and that there exists a good correlation between the capacity of LPS to suppress EAE and its mitogenic activity.
利用化学修饰衍生物,在豚鼠中研究了细菌脂多糖(LPS)诱导的对实验性变态反应性脑脊髓炎(EAE)的保护作用。LPS经羟胺分解或碱水解后,酯连接的脂肪酸从LPS中去除,导致其对B淋巴细胞的促有丝分裂活性完全丧失,同时EAE抑制活性也降低。在对髓鞘碱性蛋白(BP)的迟发型皮肤反应以及通过被动血凝和酶联免疫吸附测定(ELISA)检测到的抗BP抗体产生中,也观察到了类似的活性降低。这些结果表明,LPS抑制EAE的活性位点在脂质部分,并且LPS抑制EAE的能力与其促有丝分裂活性之间存在良好的相关性。