Riottot M M, Fournier J M, Jouin H
Infect Immun. 1981 Jan;31(1):71-7. doi: 10.1128/iai.31.1.71-77.1981.
Previous work has demonstrated the capsular serotypic specificity of the protection conferred on mice by Klebsiella pneumoniae ribosomal preparations. The data in these studies support the hypothesis that capsular polysaccharide plays at least some role in the specificity of the protection conferred by ribosomal preparations. In this investigation, the presence of capsular polysaccharide and lipopolysaccharide in K. pneumoniae ribosomal preparations was demonstrated by using immunodiffusion tests. Lipopolysaccharide content was determined for mice treated with actinomycin D. The serotype of O antigen did not play a role in the orientation of the specificity of the protection. The possibility that lipopolysaccharide might act as an adjuvant was not unlikely since the ribosomal preparations which contained the greatest amounts of lipopolysaccharide appeared to be the most immunoprotective preparations. Ribosomal preparations extracted from a noncapsulated mutant of K. pneumoniae did not protect mice. This finding suggested that capsular polysaccharide might play a role in the immunoprotective activity of ribosomes. This hypothesis was tested by using K. pneumoniae K2 bacteriophage-associated-glycanase, which specifically hydrolyzed K. pneumoniae K2 capsular polysaccharide and thereby suppressed the immunoprotective activity of K. pneumoniae K2 ribosomal preparations. In contrast, the K2 bacteriophage-associated glycanase did not interfere with the immunoprotective activity of K. pneumoniae K1 ribosomal preparations. These results clearly demonstrate that capsular polysaccharide, which is an extraribosomal antigen, is involved in the immunoprotective activity of K. pneumoniae ribosomal preparations.
先前的研究已经证明了肺炎克雷伯菌核糖体制剂对小鼠所提供保护的荚膜血清型特异性。这些研究中的数据支持这样一种假说,即荚膜多糖在核糖体制剂所提供保护的特异性中至少发挥了一定作用。在本研究中,通过免疫扩散试验证明了肺炎克雷伯菌核糖体制剂中存在荚膜多糖和脂多糖。测定了用放线菌素D处理的小鼠的脂多糖含量。O抗原的血清型在保护特异性的定向中不起作用。脂多糖可能作为佐剂的可能性并非不大,因为含有最多脂多糖的核糖体制剂似乎是最具免疫保护作用的制剂。从肺炎克雷伯菌的无荚膜突变体中提取的核糖体制剂不能保护小鼠。这一发现表明荚膜多糖可能在核糖体的免疫保护活性中发挥作用。通过使用肺炎克雷伯菌K2噬菌体相关聚糖酶对这一假说进行了验证,该酶特异性水解肺炎克雷伯菌K2荚膜多糖,从而抑制了肺炎克雷伯菌K2核糖体制剂的免疫保护活性。相比之下,K2噬菌体相关聚糖酶并不干扰肺炎克雷伯菌K1核糖体制剂的免疫保护活性。这些结果清楚地表明,作为一种核糖体外抗原的荚膜多糖参与了肺炎克雷伯菌核糖体制剂的免疫保护活性。