Marciano-Cabral Francine, Ludwick Christina, Puffenbarger Robyn A, Cabral Guy A
Department of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA 23298-0678, USA.
J Eukaryot Microbiol. 2004 Jul-Aug;51(4):472-9. doi: 10.1111/j.1550-7408.2004.tb00398.x.
Acanthamoeba spp. are opportunistic pathogens that cause granulomatous amebic encephalitis. We compared the highly pathogenic species A. culbertsoni to the relatively less pathogenic species A. castellanii for its capacity to elicit from neonatal rat microglia the gene expression of pro-inflammatory cytokines. Acanthamoeba culbertsoni elicited a robust cytokine gene response by neonatal rat microglia in vitro as compared to A. castellanii. The preponderant cytokine elicited at the mRNA and protein levels was interleukin-1beta. In addition, transmission electron microscopy revealed that microglial cells were capable of phagocytozing A. castellanii. In contrast, A. culbertsoni destroyed microglia. Collectively, these results suggest that a combined action of pro-inflammatory cytokines and destruction of host cells by amebae contribute to the pathology caused by the more pathogenic species.
棘阿米巴属是引起肉芽肿性阿米巴脑炎的机会致病菌。我们将高致病性的库氏棘阿米巴与致病性相对较低的卡氏棘阿米巴进行比较,以研究它们诱导新生大鼠小胶质细胞表达促炎细胞因子的能力。与卡氏棘阿米巴相比,库氏棘阿米巴在体外能强烈诱导新生大鼠小胶质细胞产生细胞因子基因反应。在mRNA和蛋白质水平上诱导产生的主要细胞因子是白细胞介素-1β。此外,透射电子显微镜显示小胶质细胞能够吞噬卡氏棘阿米巴。相比之下,库氏棘阿米巴会破坏小胶质细胞。总体而言,这些结果表明促炎细胞因子的联合作用以及阿米巴对宿主细胞的破坏作用导致了致病性更强的物种所引发的病理变化。