Activation of COL1A2 promoter in human fibroblasts by Escherichia coli.
Activation of COL1A2 promoter in human fibroblasts by Escherichia coli.
复制标题
大肠杆菌激活人成纤维细胞中的 COL1A2 启动子。
DOI：
10.1111/j.1574-695x.2012.00979.x
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Matsumoto T.
中科院分区：
文献类型：
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作者：
Miyazaki H;Kobayashi R;Ishikawa H;Awano N;Yamagoe S;Miyazaki Y;Matsumoto T.
使用COL 1A 2启动子转染的人成纤维细胞研究了细菌感染和胶原蛋白产生之间的关系，COL 1A 2编码人I型胶原蛋白的α1链，与荧光素酶报告基因连接。细胞用于评估细菌刺激后COL 1A 2的基因启动子活性。COL 1A 2启动子被固定的大肠杆菌以剂量依赖的方式激活，但不被固定的金黄色葡萄球菌激活。在E.大肠杆菌刺激的成纤维细胞与未刺激的成纤维细胞相比。抗人Toll样受体（TLR）4抗体和多粘菌素B均能明显阻断大肠杆菌刺激的COL 1A 2启动子活性。而抗人TLR 2抗体和抗人转化生长因子-β（TGF-β）受体II型抗体则无此作用。这些结果表明，E.大肠杆菌多糖直接与成纤维细胞表面表达的TLR 4相互作用，并可进一步诱导这些细胞中人I型胶原基因表达和胶原产生。这些数据还表明，革兰氏阴性菌感染可能导致纤维化。
The relationship between bacterial infection and collagen production was investigated using human fibroblasts transfected with the promoter ofCOL1A2, which encodes the α1 chain of human type I collagen, linked to a luciferase reporter. The cells were used to assess the gene promoter activity ofCOL1A2following bacterial stimulation. TheCOL1A2promoter was activated by stimulation with fixedEscherichia coliin a dose-dependent manner, but not by fixedStaphylococcus aureus. Enhancement of collagen production was observed in theE. coli-stimulated fibroblasts compared to those without stimulation. Both anti-human Toll-like receptor (TLR) 4 antibody and polymyxin B clearly blocked theCOL1A2promoter activity stimulated byE. coli, while antibodies against human TLR2 and human transforming growth factor-β (TGF-β) receptor type II did not. These results indicate thatE. colican directly interact with TLR4 expressed on the surface of fibroblasts and can further induce human type I collagen gene expression and collagen production in these cells. These data also suggest that infection by gram-negative bacteria may cause fibrosis.