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细胞内金黄色葡萄球菌诱导的上皮细胞基因表达

Epithelial Cell Gene Expression Induced by Intracellular Staphylococcus aureus.

作者信息

Li Xianglu, Fusco William G, Seo Keun S, Bayles Kenneth W, Mosley Erin E, McGuire Mark A, Bohach Gregory A

机构信息

Department of Microbiology, Molecular Biology and Biochemistry, University of Idaho, Moscow, ID 83844, USA.

出版信息

Int J Microbiol. 2009;2009:753278. doi: 10.1155/2009/753278. Epub 2009 Feb 3.

DOI:10.1155/2009/753278
PMID:20016671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2775199/
Abstract

HEp-2 cell monolayers were cocultured with intracellular Staphylococcus aureus, and changes in gene expression were profiled using DNA microarrays. Intracellular S. aureus affected genes involved in cellular stress responses, signal transduction, inflammation, apoptosis, fibrosis, and cholesterol biosynthesis. Transcription of stress response and signal transduction-related genes including atf3, sgk, map2k1, map2k3, arhb, and arhe was increased. In addition, elevated transcription of proinflammatory genes was observed for tnfa, il1b, il6, il8, cxcl1, ccl20, cox2, and pai1. Genes involved in proapoptosis and fibrosis were also affected at transcriptional level by intracellular S. aureus. Notably, intracellular S. aureus induced strong transcriptional down-regulation of several cholesterol biosynthesis genes. These results suggest that epithelial cells respond to intracellular S. aureus by inducing genes affecting immunity and in repairing damage caused by the organism, and are consistent with the possibility that the organism exploits an intracellular environment to subvert host immunity and promote colonization.

摘要

将人喉表皮样癌细胞单层与细胞内金黄色葡萄球菌共培养,利用DNA微阵列分析基因表达的变化。细胞内金黄色葡萄球菌影响参与细胞应激反应、信号转导、炎症、凋亡、纤维化和胆固醇生物合成的基因。应激反应和信号转导相关基因(包括atf3、sgk、map2k1、map2k3、arhb和arhe)的转录增加。此外,观察到促炎基因tnfa、il1b、il6、il8、cxcl1、ccl20、cox2和pai1的转录升高。参与促凋亡和纤维化的基因在转录水平上也受到细胞内金黄色葡萄球菌的影响。值得注意的是,细胞内金黄色葡萄球菌诱导了几个胆固醇生物合成基因的强烈转录下调。这些结果表明,上皮细胞通过诱导影响免疫和修复该生物体所造成损伤的基因来对细胞内金黄色葡萄球菌作出反应,这与该生物体利用细胞内环境来破坏宿主免疫并促进定植的可能性是一致的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09f7/2775199/fc16436372e5/IJMB2009-753278.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09f7/2775199/74aa5e0fb3e3/IJMB2009-753278.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09f7/2775199/fc16436372e5/IJMB2009-753278.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09f7/2775199/74aa5e0fb3e3/IJMB2009-753278.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09f7/2775199/fc16436372e5/IJMB2009-753278.002.jpg

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