Gitler C, Mogyoros M, Calef E, Rosenberg I
Trans R Soc Trop Med Hyg. 1985;79(5):581-6. doi: 10.1016/0035-9203(85)90162-2.
Lethal recognition between Entamoeba histolytica and the tissues and defence systems of the host results in a continuous interplay that determines the development of pathological lesions: (i) we have identified several of the steps and mediators utilized by the trophozoites to destroy host cells by contact-mediated cytolysis; (ii) we have established that the alternative complement system represents the main defence available to the host against the invading parasite. The amoebae recognize target cells by means of a lectin specific for N-acetylgalactosamine-containing surface glycoproteins. This recognition appears to activate the amoeba to release, in the area of contact, an attack complex that induces the host cells to undergo cytolysis. The main component of the attack complex is thought to be amoebapore, an ion-channel forming protein that incorporates spontaneously into target cells leading to their depolarization by creating a pathway for ions to flow down their concentration gradient. The known properties of amoebapore are described. The acquisition of complement resistance by the invading trophozoites is essential for their survival within the host and therefore underlies virulence. The resistance to complement killing is not a permanent property of the amoebae. It is lost during axenization and reappears on passage through the host or when the trophozoites are grown axenically in the presence of active complement.
溶组织内阿米巴与宿主组织及防御系统之间的致死性识别导致了一种持续的相互作用，这种相互作用决定了病理损伤的发展：（i）我们已经确定了滋养体通过接触介导的细胞溶解破坏宿主细胞所利用的几个步骤和介质；（ii）我们已经确定替代补体系统是宿主对抗入侵寄生虫的主要防御手段。变形虫通过一种对含N-乙酰半乳糖胺的表面糖蛋白具有特异性的凝集素识别靶细胞。这种识别似乎激活了变形虫，使其在接触区域释放一种攻击复合物，该复合物诱导宿主细胞发生细胞溶解。攻击复合物的主要成分被认为是溶组织内阿米巴穿孔素，一种形成离子通道的蛋白质，它会自发地整合到靶细胞中，通过为离子创造一条沿其浓度梯度流动的途径而导致靶细胞去极化。文中描述了溶组织内阿米巴穿孔素的已知特性。入侵的滋养体获得补体抗性对其在宿主体内的存活至关重要，因此是毒力的基础。对补体杀伤的抗性不是变形虫的永久特性。它在无共生培养时丧失，并在通过宿主传代时或当滋养体在活性补体存在下进行无共生培养时重新出现。
