Flores-Romo L, Estrada-García T, Shibayama-Salas M, Campos-Rodríguez R, Bacon K, Martínez-Palomo A, Tsutsumi V
Glaxo Institute for Molecular Biology, Geneva, Switzerland.
Parasitol Res. 1997;83(4):397-400. doi: 10.1007/s004360050271.
Extraintestinal dissemination of Entamoeba histolytica is frequently manifested by the life-threatening amebic liver abscess (ALA). The hepatic establishment of amebas implies invasion of blood vessels and contact with the endothelium. By means of a fluorescence-based quantitative adhesion assay, we assessed the binding to human endothelial cells of two E. histolytica strains of different virulence. The highly virulent strain (L-A) adhered substantially more strongly to unstimulated endothelium than the non-virulent one (BG3). Attachment of L-A was increased by treatment of endothelial cells with interleukin-1 beta (IL1 beta). Other proinflammatory cytokines such as interferon-gamma (IFN gamma) and tumor necrosis factor-alpha (TNF alpha) did not modify the spontaneous adhesion capacity of amebas. For purposes of comparison we also performed adhesion of the parasites to skin fibroblasts. Adhesion to this cell type was quite low (< 10%). Parasite virulence, differential adhesive capacity to endothelial cells, and modulation of the latter phenomenon by proinflammatory factors (IL1 beta) may influence the evolution and outcome of extraintestinal amebiasis, especially hepatic abscesses.
溶组织内阿米巴的肠外播散常表现为威胁生命的阿米巴肝脓肿（ALA）。阿米巴在肝脏的定植意味着血管侵袭和与内皮细胞的接触。通过基于荧光的定量黏附试验，我们评估了两种不同毒力的溶组织内阿米巴菌株与人内皮细胞的结合情况。高毒力菌株（L-A）与未刺激的内皮细胞的黏附力明显强于无毒力菌株（BG3）。用白细胞介素-1β（IL1β）处理内皮细胞可增加L-A的黏附。其他促炎细胞因子，如干扰素-γ（IFNγ）和肿瘤坏死因子-α（TNFα），不会改变阿米巴的自发黏附能力。为作比较，我们还进行了寄生虫与皮肤成纤维细胞的黏附试验。寄生虫对这种细胞类型的黏附力相当低（<10%）。寄生虫毒力、对内皮细胞的差异黏附能力以及促炎因子（IL1β）对后一种现象的调节可能会影响肠外阿米巴病的发展和结局，尤其是肝脓肿。
