Growth inhibition of Cryptococcus neoformans by human alveolar macrophages.
Growth inhibition of Cryptococcus neoformans by human alveolar macrophages.
复制标题
人肺泡巨噬细胞对新型隐球菌的生长抑制。
DOI：
10.1164/ajrccm/136.5.1242
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Koren,HS
中科院分区：
文献类型：
--
作者：
Weinberg,PB;Becker,S;Granger,DL;Koren,HS
用新生隐球菌的薄囊克隆与人肺泡巨噬细胞（AM）共培养，研究了AM对新生隐球菌的细胞毒作用。在聚丙烯培养管测定系统中。在AM的去污剂裂解后通过电子颗粒计数定量酵母复制，并通过定量平板计数定量存活力。在适当的条件下，真菌复制在人AM存在下被抑制。这种效应持续了48小时的时间进程。在此期间，单独培养基中的微生物迅速增殖，每4小时数量翻一番。人AM不需要内毒素、胎牛血清或特异性兔抗隐球菌抗体进行抑菌。在这些条件下，显微镜评价的细胞离心制备的AM-酵母共培养物，染色的修改Giemsa技术，揭示了所有的真菌是细胞外的。在10%新鲜人血清存在下，AM吞噬C.新形式并表现出杀真菌活性。肿瘤坏死因子不影响酵母菌的复制率。这些发现表明，人类AM可能至少有两种机制来保护免受C。新人类一种是血清非依赖性的和细胞外的，并导致真菌，另一种是依赖于血清因子，并导致细胞内生长抑制和可能杀死生物体。AM修订版DIS 1987; 136：1242-1247
Macrophage cytotoxicity for Cryptococcus neoformans was investigated by culturing human alveolar macrophage (AM) with a thln-capsuled clone of C. neoformans In a polypropylene culture tube assay system. Yeast replication was quantitated by electronic particle counting after detergent lysis of AM and viability by quantitative plate counts. Under appropriate conditions, fungal replication was Inhibited in the presence of human AM. This effect persisted over the 48-h time course that wasevaluated. During this period, organisms In medium alone proliferated rapidly, doubling their number every 4 h. Human AM did not require endotoxin, fetal calf serum, or specific rabbit antlcryptococcal antibody for funglstasis. Under these conditions, microscopic evaluation of a cytocentrifuge preparation of AM-yeast cocultures, stained by a modified Giemsa technique, revealed all the fungi to be extracellular. In the presence of 10% fresh human serum, AM phagocytized C. neoformans and exhibited fungicidal activity. Tumor necrosis factor did not affect the replication rate of the yeast. These findings suggest that there may be at least 2 mechanisms by which human AM protect against C. neoformans. One is serum-independent and extracellular and results in funglstasls, and the other is dependent on a serum factor and leads to intracellular inhibition of growth and possibly killing of the organism. AM REV RESPIR DIS 1987; 136: 1242-1247