Hamilton J A, Whitty G A, Last K, Royston A K, Hart P H, Burgess D R
Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Parkville, Australia.
Blood. 1992 Jul 1;80(1):121-5.
Using a specific enzyme-linked immunosorbent assay, plasminogen activator inhibitor-2 (PAI-2) was quantitated in cultures of human monocytes. Lipopolysaccharide (LPS) increased both extracellular and cell-associated PAI-2 levels, as well as PAI-2 mRNA measured by Northern analysis. Both the lymphokine, interleukin-4 (IL-4) (greater than or equal to 10 pmol/L), and the glucocorticoid, dexamethasone (100 nmol/L), inhibited PAI-2 formation and PAI-2 mRNA induction. Another lymphokine, interferon-gamma (IFN-gamma) (100 U/mL), as for IL-4 alone, did not stimulate PAI-2 formation; however, in contrast to IL-4, IFN-gamma did not reverse the LPS effect but could potentiate it. The suppression of PAI-2 formation by IL-4 and glucocorticoid in stimulated human monocytes extends the list of monocyte products whose synthesis can be downregulated in these cells by the two agents. The findings could have relevance to the control by monocytes/macrophages of connective tissue resorption, including that of fibrin, at sites of inflammation.
使用特定的酶联免疫吸附测定法，对人单核细胞培养物中的纤溶酶原激活物抑制剂-2（PAI-2）进行定量。脂多糖（LPS）增加了细胞外和细胞相关的PAI-2水平，以及通过Northern分析测定的PAI-2 mRNA水平。淋巴因子白细胞介素-4（IL-4）（≥10 pmol/L）和糖皮质激素地塞米松（100 nmol/L）均抑制PAI-2的形成和PAI-2 mRNA的诱导。另一种淋巴因子干扰素-γ（IFN-γ）（100 U/mL），与单独的IL-4一样，不刺激PAI-2的形成；然而，与IL-4相反，IFN-γ不会逆转LPS的作用，反而会增强其作用。IL-4和糖皮质激素对受刺激的人单核细胞中PAI-2形成的抑制作用，扩展了单核细胞产物的种类，这两种物质可下调这些细胞中这些产物的合成。这些发现可能与单核细胞/巨噬细胞对炎症部位结缔组织吸收（包括纤维蛋白吸收）的控制有关。
