Schwartz B S, Monroe M C, Bradshaw J D
Department of Medicine, University of Wisconsin, Madison.
Blood. 1989 Jun;73(8):2188-95.
Peripheral blood mononuclear cells (PBMs) produce both tissue factor and plasminogen activator inhibitor type 2 (PAI-2) in response to gram-negative bacterial lipopolysaccharide (LPS). The cellular roles in the tissue factor response have been previously elucidated, and we now report those roles in PAI-2 production. Monocytes are the only cells among LPS-stimulated PBMs that produce PAI-2 as assessed by measurement of PAI-2 activity and antigen. Concomitant immunohistochemistry demonstrated that monocytes contain PAI-2, with a greater number staining positively and more intensely after exposure to LPS. LPS-stimulated monocytes produced increased amounts of PAI-2 with or without addition of lymphocytes. Lymphocytes prestimulated with LPS and then washed did not induce PAI-2 production in monocytes to which they were added. Lipid X, a precursor in the biosynthetic pathway of lipid A and LPS, was able to inhibit LPS induction of monocyte PAI-2 in a dose-dependent manner. This inhibition was not due to cellular toxicity, the phospholipidlike nature of lipid X, interference with the PAI-2 assay, or monocyte production of a substance interfering with PAI-2. Lipid X was an effective inhibitor of PAI-2 production even when added up to 30 minutes after LPS.
外周血单核细胞（PBMs）在受到革兰氏阴性菌脂多糖（LPS）刺激时会产生组织因子和2型纤溶酶原激活物抑制剂（PAI-2）。此前已经阐明了细胞在组织因子反应中的作用，我们现在报告这些细胞在PAI-2产生中的作用。通过测量PAI-2活性和抗原评估，单核细胞是LPS刺激的PBMs中唯一产生PAI-2的细胞。同时进行的免疫组织化学表明，单核细胞含有PAI-2，暴露于LPS后，阳性染色的细胞数量更多且染色更强。无论是否添加淋巴细胞，LPS刺激的单核细胞都会产生更多的PAI-2。用LPS预刺激然后洗涤的淋巴细胞不会诱导与其共培养的单核细胞产生PAI-2。脂质X是脂质A和LPS生物合成途径中的前体，能够以剂量依赖的方式抑制LPS诱导的单核细胞PAI-2产生。这种抑制不是由于细胞毒性、脂质X的磷脂样性质、对PAI-2检测的干扰或单核细胞产生干扰PAI-2的物质。即使在LPS加入后30分钟再添加脂质X，它仍然是PAI-2产生的有效抑制剂。
