Marciano-Cabral F, Toney D M
Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0678, USA.
J Eukaryot Microbiol. 1998 Jul-Aug;45(4):452-8. doi: 10.1111/j.1550-7408.1998.tb05099.x.
Acanthamoeba spp. are free-living amebae associated with amebic keratitis and chronic granulomatous amebic encephalitis. The present studies were undertaken to compare the pathogenicity of three species of Acanthamoeba in B6C3F1 mice after intranasal challenge with Acanthamoeba-induced cytopathogenicity for different macrophage populations. The ability of murine macrophage cell lines and activated murine peritoneal macrophages to lyse Acanthamoeba has been assessed by coincubating macrophages with 3H-uridine labeled amebae. Conversely, destruction of macrophages by Acanthamoeba was determined by measuring the release of chromium-51 from radiolabeled macrophages. Acanthamoeba culbertsoni, which is highly pathogenic for mice, destroys macrophage cultures in vitro. Activated primary peritoneal macrophages were more resistant to Acanthamoeba-mediated destruction than macrophage cell lines activated in vitro. Activated macrophages were capable of limited destruction of Acanthamoeba polyphaga and Acanthamoeba castellanii. Acanthamoeba-specific antibodies increased the amebicidal activity of activated macrophages. Macrophage-mediated destruction was by contact-dependent cytolysis and by ingestion of amebae. Conditioned medium obtained from macrophage cultures after treatment with lipopolysaccharide and interferon gamma was neither cytolytic nor cytostatic for Acanthamoeba spp. Purified recombinant cytokines including tumor necrosis factor alpha, interleukin 1 alpha, and interleukin 1 beta, alone or in combination, were not cytolytic for Acanthamoeba trophozoites.
棘阿米巴属是与阿米巴角膜炎和慢性肉芽肿性阿米巴脑炎相关的自由生活阿米巴。本研究旨在比较鼻内接种三种棘阿米巴后,它们在B6C3F1小鼠中的致病性,以及棘阿米巴对不同巨噬细胞群体的细胞致病性。通过将巨噬细胞与3H-尿苷标记的阿米巴共同孵育,评估了小鼠巨噬细胞系和活化的小鼠腹腔巨噬细胞裂解棘阿米巴的能力。相反,通过测量放射性标记巨噬细胞中51铬的释放来确定棘阿米巴对巨噬细胞的破坏。对小鼠具有高度致病性的库氏棘阿米巴在体外可破坏巨噬细胞培养物。活化的原代腹腔巨噬细胞比体外活化的巨噬细胞系对棘阿米巴介导的破坏更具抗性。活化的巨噬细胞能够有限地破坏多食棘阿米巴和卡氏棘阿米巴。棘阿米巴特异性抗体可增强活化巨噬细胞的杀阿米巴活性。巨噬细胞介导的破坏是通过接触依赖性细胞溶解和吞噬阿米巴实现的。用脂多糖和干扰素γ处理巨噬细胞培养物后获得的条件培养基对棘阿米巴属既无细胞溶解作用也无细胞抑制作用。纯化的重组细胞因子,包括肿瘤坏死因子α、白细胞介素1α和白细胞介素1β,单独或联合使用,对棘阿米巴滋养体均无细胞溶解作用。