Meister H, Heymer B, Schäfer H, Haferkamp O
J Infect Dis. 1977 Feb;135(2):235-42. doi: 10.1093/infdis/135.2.235.
Hepatic granulomas were induced in mice by injection of blastospores, cell walls, and glucan of Candida albicans. Granulomatous reactions in liver tissue initially multiplied but later decreased. A dose-response relationship was apparent with up to 3 mg of inoculum. Shortly after injection of C. albicans spores, fungal elements appeared in liver macrophages and were detectable in granuloma and Kupffer cells for 20 days. Gram-stain, periodic acid-Schiff (PAS), and immunofluorescence reactions soon vanished, and the organisms could no longer be seen. Glucan of C. albicans, which lacked PAS and immunofluorescence reactivity, proved active in initiation of granulomas. Degradation of phagocytized spores of C. albicans, reductions of cytoplasm, and cell wall deformation and collapse support the premise that loss of PAS and immunofluorescence reactivity was caused by enzymatic breakdown of candida cell wall mannan in macrophages. We conclude that C. albicans can induce granulomatous reactions in mouse liver when the glucan that forms the cell wall matrix in Candida persists in identifiable residues.
通过注射白色念珠菌的芽生孢子、细胞壁和葡聚糖在小鼠中诱导肝肉芽肿。肝组织中的肉芽肿反应最初增加,但随后减少。接种量高达3毫克时,剂量反应关系明显。注射白色念珠菌孢子后不久,真菌成分出现在肝巨噬细胞中,并在肉芽肿和库普弗细胞中可检测到20天。革兰氏染色、过碘酸希夫(PAS)染色和免疫荧光反应很快消失,不再能看到这些生物体。缺乏PAS和免疫荧光反应性的白色念珠菌葡聚糖在肉芽肿形成中被证明具有活性。吞噬的白色念珠菌孢子的降解、细胞质的减少以及细胞壁的变形和塌陷支持了PAS和免疫荧光反应性丧失是由巨噬细胞中念珠菌细胞壁甘露聚糖的酶解作用引起的这一前提。我们得出结论,当白色念珠菌中形成细胞壁基质的葡聚糖以可识别的残基形式存在时,白色念珠菌可在小鼠肝脏中诱导肉芽肿反应。