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首页> 外文期刊>Infection and immunity >Pathogenicity of the diffusely adhering strain Escherichia coli C1845: F1845 adhesin-decay accelerating factor interaction, brush border microvillus injury, and actin disassembly in cultured human intestinal epithelial cells.
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Pathogenicity of the diffusely adhering strain Escherichia coli C1845: F1845 adhesin-decay accelerating factor interaction, brush border microvillus injury, and actin disassembly in cultured human intestinal epithelial cells.

机译：大肠杆菌C1845：F1845黏附素-衰减促进因子相互作用，刷状边界微绒毛膜损伤和肌动蛋白在培养的人肠上皮细胞中的弥散粘附株的致病性。

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The diffusely adhering Escherichia coli strain C1845 harboring the fimbrial F1845 adhesin can infect cultured human intestinal epithelial cells. The mechanism by which E. coli C1845 induces diarrheal illness remains unknown. This study investigated the injuries of cultured human intestinal cells promoted by E. coli C1845. Membrane-associated decay accelerating factor was identified as the intestinal receptor for the F1845 fimbrial adhesin of the E. coli C1845 strain by using purified F1845 adhesin, antibody directed against the F1845 adhesin, and monoclonal antibodies directed against the decay accelerating factor. Using monolayers of Caco-2 cells apically infected with E. coli C1845 and examined by scanning and transmission electron microscopy, we observed that strain C1845 induced injury to microvilli (MV) characterized by elongation and nucleation of the MV. We observed that infection of T84 and Caco-2 cells by E. coli C1845 was followed by disassembly of the actin network in the apical and basal cell domains. MV injury was differentiation related: E. coli C1845 promoted MV injury only when the cells were fully differentiated. The disassembly of the actin network occurred in poorly differentiated and fully differentiated Caco-2 cells but not in undifferentiated cells. Moreover, apical actin disassembly was observed in fully differentiated Caco-2 cells infected with the laboratory strain E. coli HB101(pSSS1) expressing the F1845 adhesin. In conclusion, E. coli C1845 promotes MV lesion in human epithelial intestinal cells, resulting from disassembly of the actin network.
机译：带有纤维F1845粘附素的弥散粘附的大肠杆菌C1845菌株可以感染培养的人肠上皮细胞。大肠杆菌C1845引起腹泻病的机制尚不清楚。这项研究调查了大肠杆菌C1845促进培养的人类肠道细胞的损伤。通过使用纯化的F1845粘附素，针对F1845粘附素的抗体和针对衰变加速因子的单克隆抗体，将膜相关的衰变促进因子鉴定为大肠杆菌C1845菌株的F1845纤维粘附素的肠受体。使用单层感染了大肠杆菌C1845的单层Caco-2细胞并通过扫描和透射电子显微镜检查，我们观察到菌株C1845诱导了以绒毛伸长和成核为特征的微绒毛（MV）损伤。我们观察到，大肠杆菌C1845感染T84和Caco-2细胞后，肌动蛋白网络在顶端和基底细胞域中被分解。 MV损伤与分化有关：只有在细胞完全分化后，大肠杆菌C1845才会促进MV损伤。肌动蛋白网络的分解发生在低分化和完全分化的Caco-2细胞中，而不发生在未分化的细胞中。此外，在感染了表达F1845粘附素的实验室菌株E. coli HB101（pSSS1）的完全分化的Caco-2细胞中观察到了顶端肌动蛋白的拆卸。总之，由于肌动蛋白网络的分解，大肠杆菌C1845促进人上皮肠道细胞的MV损伤。

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