Huang K, Fishwild D M, Wu H M, Dedrick R L
Department of Immunology, XOMA Corporation, Berkeley, California 94710, USA.
Inflammation. 1995 Jun;19(3):389-404. doi: 10.1007/BF01534395.
Endothelial cells stimulated by LPS express E-selectin, which plays an important role in mediating neutrophil adhesion during inflammation. E-selectin is induced within 1-2 h, peaks at 4-6 h, and gradually returns to basal level by 24 h. rBPI21, a recombinant N-terminal fragment of human bactericidal/permeability-increasing protein (BPI), inhibited LPS-induced E-selectin expression when added at the same time as, and up to 6 h after, LPS. Delayed administration of rBPI21 also affected LPS-mediated activation of the nuclear factor, NF-kappa B. Two to 4 h following LPS addition to endothelial cells, when NF-kappa B was already activated, addition of rBPI21 resulted in marked reduction of NF-kappa B detectable at 4 or 6 h. These results indicate that endothelial activation requires continuous presence of LPS, and rBPI21 acts to reverse LPS-mediated endothelial activation by interrupting the on-going LPS signal.
受脂多糖（LPS）刺激的内皮细胞表达E-选择素，其在炎症过程中介导中性粒细胞黏附中起重要作用。E-选择素在1 - 2小时内被诱导产生，4 - 6小时达到峰值，并在24小时时逐渐恢复至基础水平。重组人杀菌/通透性增加蛋白（BPI）的N端片段rBPI21，在与LPS同时添加以及在LPS添加后长达6小时内添加时，可抑制LPS诱导的E-选择素表达。rBPI21的延迟给药也影响LPS介导的核因子NF-κB的激活。在内皮细胞添加LPS后2至4小时，当NF-κB已经被激活时，添加rBPI21会导致在4或6小时时可检测到的NF-κB显著减少。这些结果表明内皮细胞激活需要LPS持续存在，并且rBPI21通过中断正在进行的LPS信号来逆转LPS介导的内皮细胞激活。
