Ravdin J I, Sperelakis N, Guerrant R L
J Infect Dis. 1982 Sep;146(3):335-40. doi: 10.1093/infdis/146.3.335.
Entamoeba histolytica (axenic strain HM1-IMSS), a cytolytic enteric pathogen, kills target Chinese hamster ovary cells in two discrete steps: (1) carbohydrate-specific adherence of amoebae to target cells, followed by (2) cytolysis of adherent target cells. Both steps require intact amoebic microfilament function. The effects of the fast Na+ channel blocker tetrodotoxin and the slow Na+-Ca++ channel blockers verapamil (10(-5) M) and bepridil (10(-5) M) on amoebic killing were evaluated. Verapamil and bepridil both decreased amoebic killing (P less than 0.001); tetrodotoxin had no effect. Bepridil, but not verapamil, inhibited amoebic adherence at 37 C (P less than 0.001). Both verapamil and bepridil inhibited amoebic lysis of cells after adherence occurred (P less than 0.001). Verapamil protected target cells from lysis by amoebae (P less than 0.005), whereas bepridil reduced the capacity of amoebae to kill Chinese hamster ovary cells (P less than 0.001). These findings suggest that changes in transmembrane ion flux in both the amoeba and the target cell are involved in amoebic killing of target cells.
溶组织内阿米巴（无菌株HM1-IMSS）是一种溶细胞性肠道病原体，它通过两个不同步骤杀死靶细胞中国仓鼠卵巢细胞：（1）阿米巴对靶细胞的碳水化合物特异性黏附，随后是（2）黏附的靶细胞的细胞溶解。这两个步骤都需要完整的阿米巴微丝功能。评估了快速钠离子通道阻滞剂河豚毒素以及慢速钠钙通道阻滞剂维拉帕米（10^(-5) M）和苄普地尔（10^(-5) M）对阿米巴杀伤作用的影响。维拉帕米和苄普地尔均降低了阿米巴的杀伤作用（P<0.001）；河豚毒素无作用。苄普地尔而非维拉帕米在37℃时抑制阿米巴的黏附（P<0.001）。维拉帕米和苄普地尔均在黏附发生后抑制阿米巴对细胞的溶解（P<0.001）。维拉帕米保护靶细胞免受阿米巴的溶解（P<0.005），而苄普地尔降低了阿米巴杀死中国仓鼠卵巢细胞的能力（P<0.001）。这些发现表明，阿米巴和靶细胞中跨膜离子通量的变化均参与了阿米巴对靶细胞的杀伤。
