Black C M, Beaman B L, Donovan R M, Goldstein E
Infect Immun. 1985 Feb;47(2):375-83. doi: 10.1128/iai.47.2.375-383.1985.
It has been reported that the activity of lysosomal acid phosphatase decreases inversely with numbers of ingested virulent Nocardia spp. in normal murine peritoneal and alveolar macrophages. These studies suggested that this relationship correlated with the effectiveness of these macrophage populations in killing Nocardia asteroides. Experiments were designed to determine if acid phosphatase activity is affected by infection with N. asteroides in four different macrophage populations isolated from normal and nocardia-immunized mice. Macrophages were also tested simultaneously for their ability to kill N. asteroides. Peritoneal, alveolar, and splenic macrophages and Kupffer cells were infected in vitro with strains of N. asteroides of differing virulence. Uptake and killing assays were performed. Acid phosphatase levels and numbers of intracellular nocardiae were quantitated in the same macrophages, using a computer-assisted cytophotometry system. Acid phosphatase activity decreased inversely with numbers of intracellular nocardiae in macrophages that could not kill or inhibit this pathogen. Acid phosphatase activity was not significantly changed in macrophages that inhibited growth of, but did not kill, N. asteroides, whereas activity was increased or enhanced in macrophages that killed most of the ingested nocardiae. The order of nocardicidal effectiveness (and resistance to enzyme activity reduction with infection) for normal macrophages was splenic greater than peritoneal greater than alveolar greater than Kupffer. In contrast, the order of these two parameters for macrophages isolated from immunized mice was Kupffer greater than peritoneal greater than alveolar greater than splenic. These results demonstrate that lysosomal acid phosphatase activity is an effective marker of the ability of macrophages to inhibit growth of and kill N. asteroides and that macrophages isolated from different anatomical sites differ functionally from each other with respect to nocardicidal and acid phosphatase activities.
据报道,在正常小鼠腹膜和肺泡巨噬细胞中,溶酶体酸性磷酸酶的活性与摄入的致病性诺卡氏菌属数量呈反比。这些研究表明,这种关系与这些巨噬细胞群体杀灭星形诺卡氏菌的有效性相关。设计实验以确定酸性磷酸酶活性是否受到从正常和诺卡氏菌免疫小鼠分离的四种不同巨噬细胞群体中感染星形诺卡氏菌的影响。同时还测试了巨噬细胞杀灭星形诺卡氏菌的能力。用不同毒力的星形诺卡氏菌菌株体外感染腹膜、肺泡、脾巨噬细胞和库普弗细胞。进行摄取和杀伤试验。使用计算机辅助细胞光度测量系统对同一巨噬细胞中的酸性磷酸酶水平和细胞内诺卡氏菌数量进行定量。在不能杀灭或抑制该病原体的巨噬细胞中,酸性磷酸酶活性与细胞内诺卡氏菌数量呈反比。在抑制星形诺卡氏菌生长但未将其杀灭的巨噬细胞中,酸性磷酸酶活性没有显著变化,而在杀灭了大部分摄入的诺卡氏菌的巨噬细胞中,活性增加或增强。正常巨噬细胞的杀诺卡氏菌有效性顺序(以及感染后对酶活性降低的抵抗力)为脾巨噬细胞大于腹膜巨噬细胞大于肺泡巨噬细胞大于库普弗细胞。相比之下,从免疫小鼠分离的巨噬细胞的这两个参数顺序为库普弗细胞大于腹膜巨噬细胞大于肺泡巨噬细胞大于脾巨噬细胞。这些结果表明,溶酶体酸性磷酸酶活性是巨噬细胞抑制星形诺卡氏菌生长和杀灭能力的有效标志物,并且从不同解剖部位分离的巨噬细胞在杀诺卡氏菌和酸性磷酸酶活性方面在功能上彼此不同。