Mirelman D, Feingold C, Wexler A, Bracha R
Ciba Found Symp. 1983;99:2-30. doi: 10.1002/9780470720806.ch2.
Axenically grown pathogenic and non-pathogenic isolates of Entamoeba histolytica have been shown to adhere to mammalian epithelial cells and bacteria by virtue of carbohydrate-binding proteins present on their cell surfaces. The interaction of amoeba isolates of low pathogenicity with a variety of gram-negative bacteria, mainly Escherichia coli strains which are readily ingested by the amoebae after relatively short periods, significantly increased the ability of the trophozoites to: (a) destroy and ingest intestinal epithelial cells; (b) secrete a cytopathic substance which morphologically affects a variety of tissue-cultured cells; and (c) cause hepatic abscesses in hamsters. Addition of carbohydrates that inhibit the lectin-mediated attachment of bacteria to amoebae prevented the enhancement of virulence. Interaction of the amoebae with bacteria that were heat-inactivated, glutaraldehyde-fixed or disrupted by sonication, as well as with bacteria precoated with antibodies or concanavalin A, did not lead to an increase in virulence. Moreover, short prior treatments of the bacteria with inhibitors of protein synthesis, but not with cell-wall synthesis inhibitors, also prevented the stimulation. The results indicate that interactions of amoebae with certain bacteria may be responsible for the increase in amoebic virulence.
已证明,无菌培养的致病性和非致病性溶组织内阿米巴分离株可凭借其细胞表面存在的碳水化合物结合蛋白黏附于哺乳动物上皮细胞和细菌。低致病性的阿米巴分离株与多种革兰氏阴性菌相互作用,主要是大肠杆菌菌株,这些细菌在较短时间后很容易被阿米巴摄取,这显著增强了滋养体的以下能力:(a) 破坏并摄取肠道上皮细胞;(b) 分泌一种对多种组织培养细胞有形态学影响的细胞致病物质;(c) 在仓鼠体内引起肝脓肿。添加抑制凝集素介导的细菌与阿米巴黏附的碳水化合物可阻止毒力增强。阿米巴与经热灭活、戊二醛固定或超声破碎的细菌以及与预先包被抗体或伴刀豆球蛋白A的细菌相互作用,不会导致毒力增加。此外,先用蛋白质合成抑制剂而非细胞壁合成抑制剂对细菌进行短期处理,也可阻止这种刺激。结果表明,阿米巴与某些细菌的相互作用可能是阿米巴毒力增加的原因。