Leitch Gordon J, Ward Tarsha L, Shaw Andrew P, Newman Gale
Department of Physiology, Morehouse School of Medicine, 720 Westview Dr., Atlanta, GA 30310, USA.
Infect Immun. 2005 Nov;73(11):7697-704. doi: 10.1128/IAI.73.11.7697-7704.2005.
Encephalitozoon intestinalis is a microsporidian species that infects the intestinal mucosal epithelium, primarily in immunodeficient individuals. The present study employed undifferentiated and differentiated human colonic carcinoma cell lines to determine if this parasite species infected polarized epithelial cells by spore phagocytosis or by impalement with the deployed spore polar tube. Apical surface spore attachment differed between cell lines such that SW480>HT-29>Caco-2>HCT-8, with attachment being greater to undifferentiated Caco-2 cells than differentiated cells and greater to partially differentiated HCT-8 cells than differentiated HCT-8 cells. Attachment was inhibited by chondroitin sulfate A, suggesting that it was mediated by host cell sulfated glycoaminoglycans. Infection rates 3 days postinfection paralleled spore attachment in the various cell lines. The undifferentiated cell line SW480 and undifferentiated Caco-2 and HCT-8 cells exhibited modest spore phagocytosis while the more differentiated cell line HT29 and differentiated Caco-2 and HCT-8 cells did not. All cell lines were impaled by the polar tubes of germinating spores. When normalized to the number of spores attached to the apical membrane, such impalement was greatest in the more differentiated Caco-2 and HCT-8 cells. The host cell apical surface influenced parasite spore germination, as in populations of large undifferentiated Caco-2 cells to which >3 spores had attached, the frequency distribution of the percentages of spores germinated per cell was bimodal, indicating that the surface of some cells favored germination, while others did not. This study suggests that phagocytosis is not a biologically significant mode of infection in differentiated intestinal epithelial cells.
肠脑炎微孢子虫是一种微孢子虫物种,主要感染免疫功能低下个体的肠道黏膜上皮。本研究使用未分化和分化的人结肠癌细胞系,以确定该寄生虫物种是通过孢子吞噬作用还是通过已伸出的孢子极管刺入来感染极化上皮细胞。细胞系之间顶端表面的孢子附着情况不同,即SW480>HT - 29>Caco - 2>HCT - 8,未分化的Caco - 2细胞比分化细胞的附着情况更好,部分分化的HCT - 8细胞比分化的HCT - 8细胞的附着情况更好。硫酸软骨素A可抑制附着,这表明其由宿主细胞硫酸化糖胺聚糖介导。感染后3天的感染率与各细胞系中的孢子附着情况相似。未分化的细胞系SW480以及未分化的Caco - 2和HCT - 8细胞表现出适度的孢子吞噬作用,而分化程度更高的细胞系HT29以及分化的Caco - 2和HCT - 8细胞则没有。所有细胞系都被萌发孢子的极管刺入。当以附着于顶端膜的孢子数量进行标准化时,这种刺入在分化程度更高的Caco - 2和HCT - 8细胞中最为明显。宿主细胞顶端表面影响寄生虫孢子的萌发,如在附着了>3个孢子的未分化大Caco - 2细胞群体中,每个细胞萌发孢子百分比的频率分布呈双峰,表明一些细胞表面有利于萌发,而另一些则不然。本研究表明,吞噬作用在分化的肠道上皮细胞中不是一种具有生物学意义的感染方式。