Nakamura T
Mycopathologia. 1984 Apr 15;85(3):129-44. doi: 10.1007/BF00440942.
The present experiment was performed in order to analyze and compare the histopathological features of Candida infection in various states of host defense capacity. The pulmonary lesions were induced by an intratracheal inoculation of 10(8) live cells of Candida albicans into each of the rabbits in the following 4 groups: 1) untreated controls, 2) animals sensitized non-specifically to bovine serum albumin (BSA), 3) those sensitized specifically to formalin-killed C. albicans cells, and 4) those treated with cyclophosphamide and mitomycin C. The animals were sacrificed at appropriate intervals up to 16 days after inoculation. At autopsy, the lungs were cultured and then subjected to histopathological, electron microscopic and enzyme cytochemical examinations. In the healthy control animals, the fungal lesions consisted of polymorphonuclear leukocytes (PMN) at the initial stage, gradually changing to granulomatous inflammation, which contained no peroxidase-positive macrophages. In the animals sensitized non-specifically to BSA exudative macrophages appeared in the lesions, the nature of which did not differ from that of the control animals. In the animals sensitized specifically to Candida cells, more extensive infiltration of PMN was observed at the initial stage, a fact which may suggest the participation of the Arthus phenomenon in the development of the lesions. Furthermore, an epithelioid cell transformation of the macrophages in the granulomatous lesions may also suggest that immune complexes contributed to their formation. In the drug-treated animals, the lesions consisted of necrotic or less prominent cellular foci which correspond to the features of human candidiasis in debilitated states, and the inoculated fungi grew progressively to form pseudohyphae. An asteroid structure protruding radially from the surface of the fungal cells and attaching to primary lysosomes in the phagocytes was observed occasionally. This structure seems to be formed when the function of the phagocytes in the defense mechanisms against the fungi is suppressed to some extent. From the results of the present experiment, we would emphasize that PMN play an initial role in the elimination of C. albicans cells in the lung, and that macrophages then contribute to the formation of the lesions immunologically or non-immunologically.
进行本实验是为了分析和比较宿主防御能力处于不同状态时白色念珠菌感染的组织病理学特征。通过气管内接种10(8)个白色念珠菌活细胞，在以下4组兔子中诱导肺部病变：1) 未处理的对照组；2) 对牛血清白蛋白（BSA）进行非特异性致敏的动物；3) 对福尔马林灭活的白色念珠菌细胞进行特异性致敏的动物；4) 用环磷酰胺和丝裂霉素C处理的动物。在接种后长达16天的适当时间间隔处死动物。尸检时，对肺进行培养，然后进行组织病理学、电子显微镜和酶细胞化学检查。在健康对照动物中，真菌病变在初始阶段由多形核白细胞（PMN）组成，逐渐转变为肉芽肿性炎症，其中不含过氧化物酶阳性巨噬细胞。在对BSA进行非特异性致敏的动物中，病变中出现渗出性巨噬细胞，其性质与对照动物无异。在对念珠菌细胞进行特异性致敏的动物中，初始阶段观察到PMN更广泛的浸润，这一事实可能表明Arthus现象参与了病变的发展。此外，肉芽肿病变中巨噬细胞的上皮样细胞转化也可能表明免疫复合物促成了它们的形成。在药物处理的动物中，病变由坏死或不太明显的细胞灶组成，这与衰弱状态下人类念珠菌病的特征相符，接种的真菌逐渐生长形成假菌丝。偶尔观察到一种从真菌细胞表面径向突出并附着于吞噬细胞中初级溶酶体的星状结构。当吞噬细胞在抗真菌防御机制中的功能受到一定程度抑制时，似乎会形成这种结构。根据本实验结果，我们强调PMN在清除肺部白色念珠菌细胞中起初始作用，随后巨噬细胞在免疫或非免疫方面促成病变的形成。
