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肺炎克雷伯菌O3脂多糖的佐剂活性:伴刀豆球蛋白A对其佐剂活性的抑制作用

Adjuvant activity of Klebsiella O3 lipopolysaccharide: inhibition of the adjuvant activity by concanavalin A.

作者信息

Kato N, Kido N, Ohta M, Naito S

出版信息

Microbiol Immunol. 1985;29(3):205-11. doi: 10.1111/j.1348-0421.1985.tb00820.x.

Abstract

Klebsiella O3 lipopolysaccharide (KO3 LPS) was found to exhibit extraordinarily strong adjuvant activity in augmenting antibody responses and delayed-type hypersensitivity (DTH) to protein antigens in mice. The O-specific polysaccharide chain of KO3 LPS consists of alpha-mannoside. We investigated the effect of concanavalin A (Con A) or succinyl Con A, which is known to bind to alpha-mannoside, on the adjuvant activity of KO3 LPS in augmenting DTH to ovalbumin. When KO3 LPS was mixed with Con A prior to injection, the strong adjuvant activity of KO3 LPS in augmenting DTH was inhibited and the degree of inhibition depended upon the dose of Con A. An equal amount of Con A elicited nearly complete inhibition of the adjuvant activity of KO3 LPS, Con A at 1/10 the amount of LPS elicited partial inhibition, and Con A at 1/100 the amount of LPS showed no inhibition. An equal amount of succinyl Con A, which induced less marked aggregation of KO3 LPS than Con A, elicited inhibition of the adjuvant activity of KO3 LPS to an extent similar to that by Con A. On the other hand, Con A or succinyl Con A bound to KO3 LPS did not impair in any way the lethal toxicity of KO3 LPS for mice which is known to be due to the lipid A moiety. From these findings it is concluded that the strong adjuvant activity of KO3 LPS does not solely depend upon the lipid A moiety but the O-specific polysaccharide moiety plays an important role in expression of the adjuvant activity.

摘要

肺炎克雷伯菌O3型脂多糖(KO3 LPS)被发现具有极强的佐剂活性,可增强小鼠对蛋白质抗原的抗体反应和迟发型超敏反应(DTH)。KO3 LPS的O特异性多糖链由α-甘露糖苷组成。我们研究了已知能与α-甘露糖苷结合的伴刀豆球蛋白A(Con A)或琥珀酰Con A对KO3 LPS增强对卵清蛋白DTH的佐剂活性的影响。在注射前将KO3 LPS与Con A混合时,KO3 LPS增强DTH的强佐剂活性受到抑制,抑制程度取决于Con A的剂量。等量的Con A几乎完全抑制了KO3 LPS的佐剂活性,LPS量1/10的Con A引起部分抑制,而LPS量1/100的Con A则无抑制作用。等量的琥珀酰Con A诱导的KO3 LPS聚集比Con A少,其对KO3 LPS佐剂活性的抑制程度与Con A相似。另一方面,与KO3 LPS结合的Con A或琥珀酰Con A丝毫没有损害KO3 LPS对小鼠的致死毒性,已知这种致死毒性是由脂质A部分引起的。从这些发现可以得出结论,KO3 LPS的强佐剂活性并非仅取决于脂质A部分,而是O特异性多糖部分在佐剂活性的表达中起重要作用。

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