RT期刊文章SR电子T1各种脂多糖从肺上皮细胞和成纤维细胞释放单核细胞趋化活性的潜力188bet官网地址A1 Nomura，H a1 kubo，k a1 miura，m a1 yamashita，t a1 nagai，s a1 izumi，t yr 1999 ul http：//www.qdcxjkg.com/content/content/14/3/3/3/545.Abstract虽然细胞毒性毒性源自铜绿假单胞菌的脂多糖（LPS），即limulus amoebocyte裂解物活性，不如大肠杆菌0127：B8，P. eruginosa诱发了显着的持续性肺部炎症，如囊肿纤维化。本研究旨在检查从大肠杆菌和铜绿假单胞菌获得的几种LPS的潜力，以从肺细胞释放单核细胞趋化活性（MCA）。LPS差异刺激了A549细胞，BEAS-2B细胞和肺成纤维细胞，以释放MCA（P. eruginosa>e。Coli0127：B8，来自DIFCO> 055：B5，来自Sigma> 026：B6（Sigma））。大肠杆菌0127：B8（Sigma）和0111：B4（Sigma）没有刺激这些细胞。MCA是通过棋盘分析确定的。分子筛色谱柱色谱法揭示了四个趋化峰。MCA的释放被环己酰亚胺和脂氧合酶抑制剂抑制。封闭抗体的实验表明，大部分MCA继发于单核细胞趋化蛋白-1（MCP-1）和粒细胞巨噬细胞刺激因子（GM-CSF）。 Thus, the concentrations of these chemoattractants were examined and it was found that the potency of the various LPSs to stimulate MCA closely paralleled their potency in releasing MCP-1 and GM-GSF. Serum augmented the release of MCP-1 and GM-CSF. However, the differences among LPSs from E. coli and P. aeruginosa in stimulating A549 cells were observed. These data suggest that Pseudomonas aeruginosa lipopolysaccharide may stimulate lung cells to release more monocyte chemotactic activity than lipopolysaccharides derived from Escherichia coli, leading to sustained prominent lung inflammation.