白三烯B4和前列腺素E2对淋巴细胞与内皮细胞黏附的影响。
Effect of leukotriene B4 and prostaglandin E2 on the adhesion of lymphocytes to endothelial cells.
作者信息
To S S, Schrieber L
机构信息
Sydney University Department of Rheumatology, Royal North Shore Hospital, Australia.
出版信息
Clin Exp Immunol. 1990 Jul;81(1):160-5. doi: 10.1111/j.1365-2249.1990.tb05308.x.
The arachidonic acid metabolites leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) may play an important role in inflammation. It is not known whether these mediators influence the binding of lymphocytes to endothelial cells, a process which is important in the extravasation of lymphocytes in inflammatory states. In the present investigation, the effect of LTB4 and PGE2 on the binding interaction between lymphocytes and endothelial cells was examined using a centrifugation cell binding assay. Although LTB4 elicited an aggregation response on human polymorphonuclear leucocytes (PMNL) and enhanced their binding to endothelial cells it had no effect on lymphocyte binding. By contrast, PGE2 caused a dose-dependent inhibition of lymphocyte binding to endothelial cells. The inhibitory effect of PGE2 had a rapid onset but was exhibited only when PGE2 was present continuously during the cell binding assay. Although the mechanism by which PGE2 acts is not clear, it may provide a negative feedback mechanism in regulating the influx of lymphocytes into inflammatory sites.
花生四烯酸代谢产物白三烯B4（LTB4）和前列腺素E2（PGE2）可能在炎症中起重要作用。尚不清楚这些介质是否会影响淋巴细胞与内皮细胞的结合，这一过程在炎症状态下淋巴细胞外渗中很重要。在本研究中，使用离心细胞结合试验检测了LTB4和PGE2对淋巴细胞与内皮细胞之间结合相互作用的影响。尽管LTB4对人多形核白细胞（PMNL）引发了聚集反应并增强了它们与内皮细胞的结合，但对淋巴细胞结合没有影响。相比之下，PGE2引起淋巴细胞与内皮细胞结合的剂量依赖性抑制。PGE2的抑制作用起效迅速，但仅在细胞结合试验期间持续存在PGE2时才表现出来。尽管PGE2的作用机制尚不清楚，但它可能在调节淋巴细胞流入炎症部位方面提供一种负反馈机制。
Zotero 插件