Silva C L, Ekizlerian S M, Fazioli R A
Am J Pathol. 1985 Feb;118(2):238-47.
The subcutaneous, intradermal, and pulmonary inflammatory lesions induced in mice by viable Mycobacterium bovis (BCG) with no glycolipid cord factor (CF) on the outer cell wall (delipidated BCG, dBCG) was drastically different from that induced by inoculation with intact bacteria. The reaction caused by dBCG was of an acute nature: the cells making up the inflammatory infiltrate exhibited polymorphonuclear-like (PMNs) morphologic characteristics, there was a decrease on delayed hypersensitivity response, and the lesion was resolved around the 16th day after inoculation. Complete disappearance of viable organisms from the lungs, liver, and spleen of these animals occurred in parallel with the dissipation of the dBCG-induced inflammatory infiltrate, showing that CF plays an important role in the host-parasite relationship that takes place in infections caused by mycobacteria. In addition, when deprived of this glycolipid component, bacilli lose their immunostimulant ability.
在外细胞壁上没有糖脂索状因子（CF）的活牛分枝杆菌（卡介苗，BCG）诱导的小鼠皮下、皮内和肺部炎症病变与接种完整细菌诱导的病变截然不同。去脂卡介苗（dBCG）引起的反应具有急性性质：构成炎性浸润的细胞表现出多形核样（PMN）形态特征，迟发型超敏反应降低，接种后约第16天病变消退。这些动物的肺、肝和脾中活生物体的完全消失与dBCG诱导的炎性浸润的消散同时发生，表明CF在分枝杆菌引起的感染中发生的宿主-寄生虫关系中起重要作用。此外，当缺乏这种糖脂成分时，杆菌失去其免疫刺激能力。
