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首页> 外文期刊>Infection and immunity >CD14- and Toll-Like Receptor-Dependent Activation of Bladder Epithelial Cells by Lipopolysaccharide and Type 1 Piliated Escherichia coli
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CD14- and Toll-Like Receptor-Dependent Activation of Bladder Epithelial Cells by Lipopolysaccharide and Type 1 Piliated Escherichia coli

机译：CD14和类似收费的受体依赖脂多糖和1型胆管大肠杆菌激活的膀胱上皮细胞。

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The gram-negative bacterium Escherichia coli is the leading cause of urinary tract infection. The interaction between type 1 piliated E. coli and bladder epithelial cells leads to the rapid production of inflammatory mediators, such as interleukin-6 (IL-6) and IL-8. Conflicting reports have been published in the literature regarding the mechanism by which uroepithelial cells are activated by type 1 piliated E. coli. In particular, the role of lipopolysaccharide (LPS) in these responses has been an area of significant debate. Much of the data arguing against LPS-mediated activation of bladder epithelial cells have come from studies using a renal epithelial cell line as an in vitro model of the urinary epithelium. In this report, we analyzed three bladder epithelial cell lines and demonstrated that they all respond to LPS. Furthermore, the LPS responsivity of the cell lines directly correlated with their ability to generate IL-6 after E. coli stimulation. The LPS receptor complex utilized by the bladder epithelial cell lines included CD14 and Toll-like receptors, and signaling involved the activation of NF-κB and p38 mitogen-activated protein kinase. Also, reverse transcription-PCR analysis demonstrated that bladder epithelial cells express CD14 mRNA. Thus, the molecular machinery utilized by bladder epithelial cells for the recognition of E. coli is very similar to that described for traditional innate immune cells, such as macrophages. In contrast, the A498 renal epithelial cell line did not express CD14, was hyporesponsive to LPS stimulation, and demonstrated poor IL-6 responses to E. coli.
机译：革兰氏阴性细菌大肠杆菌是泌尿道感染的主要原因。类型1的 E之间的相互作用。大肠杆菌和膀胱上皮细胞可快速产生炎性介质，例如白介素6（IL-6）和IL-8。在文献中已发表了有关由1型毛细血管内皮细胞激活尿道上皮细胞的机制的矛盾报道。大肠杆菌。特别是，脂多糖（LPS）在这些反应中的作用一直是一个有争议的领域。关于LPS介导的膀胱上皮细胞激活的许多数据来自使用肾上皮细胞系作为泌尿上皮细胞体外模型的研究。在本报告中，我们分析了三种膀胱上皮细胞系，并证明它们均对LPS产生反应。此外，细胞系的LPS响应性与它们在 E后产生IL-6的能力直接相关。大肠杆菌刺激。膀胱上皮细胞系利用的LPS受体复合物包括CD14和Toll样受体，信号传导涉及NF-κB和p38丝裂原活化蛋白激酶的激活。同样，逆转录-PCR分析表明膀胱上皮细胞表达CD14 mRNA。因此，膀胱上皮细胞利用分子机制识别 E。大肠杆菌与传统的先天免疫细胞（例如巨噬细胞）所描述的非常相似。相反，A498肾上皮细胞系不表达CD14，对LPS刺激反应低下，并表现出对 E的不良IL-6反应。大肠杆菌。

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