Kato N, Kato O, Nakashima I
Jpn J Microbiol. 1976 Jun;20(3):163-72. doi: 10.1111/j.1348-0421.1976.tb00971.x.
When Klebsiella pneumoniae capsular polysaccharide (CPS-K) from type 1, Kasuya strain, was injected intraperitoneally (i.p.) immediately before i.p. bacterial challenge, the survival time of mice infected with Salmonella enteritidis NUB 1 (virulent strain) was shortened and the mortality rate for mice infected with S. enteritidis NUB 31 (avirulent strain) was enhanced. The promotion of infection with S. enteritidis NUB 1 by CPS-K depended upon its dose, the effect of CPS-K being demonstrable up to as little as 0.2 mug per mouse. In the case of S. enteritidis NUB 31, the effect of CPS-K was detectable only when more than 20 mug per mouse was injected. As a result of enumeration of bacterial populations in the peritoneal washing, blood, liver and spleen, it was revealed that CPS-K promoted in vivo growth of S. enteritidis NUB 1 and NUB 31. In addition, CPS-K enhanced the mortality rate in mice infected with Streptococcus pyogenes or Streptococcus pneumoniae. The peak CPS-K effect on infection with S. enteritidis NUB 1 was seen when given immediately before bacterial challenge. The active substance responsible for the infection-promoting effect of CPS-K was neutral CPS-K, which is distinct from the O antigen and from acidic CPS-K (the type-specific capsular antigen). Preparations of neutral CPS-K isolated from the other three strains of K. pneumoniae exhibited a marked infection-promoting effect comparable with that of preparations from the Kasuya strain. Neutral CPS-K, with identical antigenicity to that from the Kasuya strain, has already been found to exert a strong adjuvant effect on antibody responses to various antigens in mice. No parallelism exists between infection-promoting activity and adjuvant activity of neutral CPS-K.
当1型Kasuya菌株的肺炎克雷伯菌荚膜多糖(CPS-K)在腹腔注射细菌攻击前立即进行腹腔内(i.p.)注射时,感染肠炎沙门氏菌NUB 1(强毒株)的小鼠存活时间缩短,而感染肠炎沙门氏菌NUB 31(无毒株)的小鼠死亡率增加。CPS-K对肠炎沙门氏菌NUB 1感染的促进作用取决于其剂量,每只小鼠低至0.2微克的CPS-K仍可显示出效果。对于肠炎沙门氏菌NUB 31,仅当每只小鼠注射超过20微克时才能检测到CPS-K的作用。通过对腹腔冲洗液、血液、肝脏和脾脏中的细菌数量进行计数,发现CPS-K促进了肠炎沙门氏菌NUB 1和NUB 31在体内的生长。此外,CPS-K提高了感染化脓性链球菌或肺炎链球菌的小鼠的死亡率。在细菌攻击前立即给予CPS-K时,对肠炎沙门氏菌NUB 1感染的CPS-K效应达到峰值。负责CPS-K感染促进作用的活性物质是中性CPS-K,它与O抗原和酸性CPS-K(型特异性荚膜抗原)不同。从其他三株肺炎克雷伯菌分离的中性CPS-K制剂表现出与Kasuya菌株制剂相当的显著感染促进作用。已发现与Kasuya菌株具有相同抗原性的中性CPS-K对小鼠对各种抗原的抗体反应具有强烈的佐剂作用。中性CPS-K的感染促进活性和佐剂活性之间不存在平行关系。