Huang K, Conlon P J, Fishwild D M
Department of Immunology, XOMA Corporation, Berkeley, California 94710, USA.
Shock. 1994 Feb;1(2):81-6. doi: 10.1097/00024382-199402000-00001.
Exposure of cultured human umbilical vein endothelial cells (HUVEC) to lipopolysaccharide (LPS) or interleukin 1 (IL-1) causes increased expression of adhesion molecules such as E-selectin and CD54 by HUVEC and consequently increased adherence of peripheral blood neutrophils. A recombinant aminoterminal fragment of bactericidal/permeability increasing protein (rBPI23) was shown to specifically block the LPS-induced adhesiveness of HUVEC for neutrophils. rBPI23 also prevented the LPS- but not IL-1 beta-induced upregulation on HUVEC of E-selectin and CD54. Furthermore, this inhibition was evident even when the endothelial cells were exposed to LPS for up to 1-2 h prior to rBPI23 addition. The inhibitory effects of an anti-CD14 monoclonal antibodies (mAb) were similar to those of rBPI23. Combination of the anti-CD14 mAb and rBPI23 resulted inhibition greater than either one used alone. These studies demonstrate that rBPI23 acts as a specific and potent inhibitor of soluble CD14-mediated LPS induction.
将培养的人脐静脉内皮细胞（HUVEC）暴露于脂多糖（LPS）或白细胞介素1（IL-1）会导致HUVEC中E-选择素和CD54等黏附分子的表达增加，从而导致外周血中性粒细胞的黏附增加。杀菌/通透性增加蛋白的重组氨基末端片段（rBPI23）被证明可特异性阻断LPS诱导的HUVEC对中性粒细胞的黏附性。rBPI23还可防止LPS诱导的E-选择素和CD54在HUVEC上的上调，但不能防止IL-1β诱导的上调。此外，即使在内皮细胞在添加rBPI23之前暴露于LPS长达1-2小时的情况下，这种抑制作用也很明显。抗CD14单克隆抗体（mAb）的抑制作用与rBPI23相似。抗CD14 mAb和rBPI23的联合使用产生的抑制作用大于单独使用其中任何一种。这些研究表明，rBPI23作为可溶性CD14介导的LPS诱导的特异性强效抑制剂发挥作用。
