Department of Bacteriology and Immunology, The Harvard Medical School, Boston.
J Exp Med. 1936 Aug 31;64(3):425-38. doi: 10.1084/jem.64.3.425.
Since there is no evidence for the occurrence of type specific antibody in the normal rabbit and since, as we have shown, the Pneumococcus Type III whether avirulent or virulent is not removed from the blood stream or destroyed when the capsule is intact, the following factors which have been revealed in the course of our work appear to represent certain essential components, if not the complete mechanism, upon which the natural immunity of the rabbit against this organism depends. (a) The elevation of the body temperature after intravenous infection to 41 degrees C. or thereabouts and its maintenance for varying periods. (b) The ability of the phagocytic cells, both fixed and mobile, to attack any cocci which have become vulnerable through the deterioration of capsular integrity. (c) The adjuvant effect of an antibody, reacting with the somatic C carbohydrate, which enhances the phagocytosis of such organisms as no longer possess a completely intact envelope. Conversely, the varying degrees of virulence for rabbits observed among Pneumococcus Type III strains are based upon: (a) differences in the ability of the organisms to multiply at the elevated temperatures encountered in the infected host. Strains markedly susceptible to the harmful influence of this factor fail to induce a generalized fatal infection. Not all "thermo-resistant" strains are highly virulent, however, and these may contrast sharply with regard to (b) size of the capsule and the ease with which it is impaired or completely lost. The capsules must be maintained intact for a sufficient time until multiplication of the organisms can proceed to such a degree that death of the host results. Avirulent strains even when capable of growth at 41 degrees C. appear to be unable to satisfy this requirement. The differences in virulence of various strains apparently conditioned by these factors are not limited solely to the case of the rabbit, since for at least two strains similar differences in virulence have been shown to exist when the intravenous route of infection is employed in mice.
由于正常兔体内不存在型特异性抗体,而且正如我们所表明的,无论肺炎球菌 III 型是否有毒力,只要荚膜完整,它就不会从血流中清除或被破坏,因此,在我们的工作过程中发现的以下因素似乎代表了某些必要的组成部分,如果不是完整的机制,那么兔对这种生物体的自然免疫力就取决于此。(a) 静脉感染后体温升高至 41 摄氏度左右,并持续一段时间。(b) 吞噬细胞(固定的和移动的)攻击任何因荚膜完整性恶化而变得脆弱的球菌的能力。(c) 与体细胞 C 多糖反应的抗体的佐剂效应,增强了对不再具有完整包膜的此类生物体的吞噬作用。相反,肺炎球菌 III 型菌株在兔中观察到的不同毒力程度基于:(a) 生物体在感染宿主中遇到的升高温度下繁殖的能力差异。对这种因素的有害影响明显敏感的菌株不能引起全身性致命感染。并非所有“耐热”菌株都具有高度毒力,然而,这些菌株在(b) 荚膜的大小及其受损或完全丧失的容易程度方面可能存在显著差异。荚膜必须保持完整足够长的时间,直到生物体能够繁殖到导致宿主死亡的程度。即使能够在 41 摄氏度下生长的无毒菌株似乎也无法满足这一要求。各种菌株的毒力差异显然受这些因素的影响,不仅限于兔的情况,因为至少有两种菌株在静脉内感染途径用于小鼠时,已显示出类似的毒力差异。