Espinosa-Cantellano M, Martínez-Palomo A
Center for Research and Advanced Studies, Mexico City, Mexico.
Clin Microbiol Rev. 2000 Apr;13(2):318-31. doi: 10.1128/CMR.13.2.318.
In spite of a wealth of knowledge on the biochemistry and cellular and molecular biology of Entamoeba histolytica, little has been done to apply these advances to our understanding of the lesions observed in patients with intestinal amebiasis. In this review, the pathological and histological findings in acute amebic colitis are related to the molecular mechanisms of E. histolytica pathogenicity described to date. Infection of the human colon by E. histolytica produces focal ulceration of the intestinal mucosa, resulting in dysentery (diarrhea with blood and mucus). Although a complete picture has not yet been achieved, the basic mechanisms involved in the production of focal lytic lesions include complex multifactorial processes in which lectins facilitate adhesion, proteases degrade extracellular matrix components, porins help nourish the parasite and may also kill incoming polymorphonuclear leukocytes and macrophages, and motility is used by the parasite to invade deeper layers of the colon. In addition, E. histolytica has developed mechanisms to modulate the immune response during acute infection. Nevertheless, much still needs to be unraveled to understand how this microscopic parasite has earned its well-deserved histolytic name.
尽管对溶组织内阿米巴的生物化学、细胞生物学和分子生物学已有丰富的知识，但在将这些进展应用于我们对肠道阿米巴病患者所观察到的病变的理解方面，所做的工作却很少。在这篇综述中，急性阿米巴结肠炎的病理和组织学发现与迄今所描述的溶组织内阿米巴致病性的分子机制相关。溶组织内阿米巴感染人类结肠会导致肠黏膜局灶性溃疡，进而引发痢疾（伴有血液和黏液的腹泻）。尽管尚未完全明晰整个过程，但产生局灶性溶解病变所涉及的基本机制包括复杂的多因素过程，其中凝集素促进黏附，蛋白酶降解细胞外基质成分，孔蛋白有助于滋养寄生虫，还可能杀死进入的多形核白细胞和巨噬细胞，而寄生虫利用运动性侵入结肠更深层。此外，溶组织内阿米巴已形成在急性感染期间调节免疫反应的机制。然而，要理解这种微观寄生虫是如何名副其实地获得其溶组织的名称，仍有许多需要阐明的地方。
