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肿瘤坏死因子（ＴＮＦ）对外周中性粒细胞（ＰＭＮ）具有重要调节作用。本文采用生化及放射免疫技术，观察体外重组ＴＮＦ对ＰＭＮ趋化、粘附及血栓素Ｂ２（ＴＸＢ２）和前列环素（６－ＫｅｔｏｐｏＦ１ａ）释放的改变。ＴＮＦ（１００ｎｇ／ｍｌ）处理６０ｍｉｎ后，ＰＭＮ对白细胞趋化因子（ＦＭＬＰ）趋化和玻璃珠粘附性均显著增加，同时伴有ＴＸＢ２释放增多，６－Ｋｅｔｏ－ＰＧＦ１ａ不变。这提示ＴＮＰ体外促ＰＭＮ趋化和粘附可能同ＴＸＢ２相关，ＴＸＢ２／６－Ｋｅｔｏ－ＰＧＦ１ａ比值升高可能反应ＰＭＮＰＬＡ２活性有所加强。ＰＬＡ２代谢产物花生四烯酸（ＡＡ）处理６０ｍｉｎ后，ＰＭＮ趋化和粘附性也显著增加，并伴有ＴＸＢ２释放增多。ＰＬＡ２抑制剂ＰＢＰＢ可大部阻断ＴＮＦ诱导的ＰＭＮ趋化和粘附增加，而环氧化物酶抑制剂氯苯甲酰吲哚乙酸（ＩＮＤ）对ＴＮＦ诱导的上述ＰＭＮ功能无显著影响。ＰＬＡ２激活可能介导ＴＮＦ对ＰＭＮ的趋化和粘附的调节。使用ＰＬＡ２阻断剂可能阻断ＴＮＦ对ＰＭＮ的激活，减轻炎症反应造成的机体损伤。
Tumor necrosis factor (TNF) plays an important regulatory role on peripheral neutrophils (PMNs). In this paper, biochemical and radioimmunoassay techniques were used to observe the effects of recombinant TNF in vitro on the chemotaxis and adhesion of PMN and the release of TXB2 and 6-KetopoF1a. After treatment with TNF (100ng / ml) for 60min, the chemotaxis and the adhesion of leucocyte chemotactic factor (FMLP) to PMML were significantly increased, accompanied by increased TXB2 release and unchanged 6-Keto-PGF1a. This suggests that TNP in vitro promote PMN chemotaxis and adhesion may be associated with TXB2, TXB2 / 6-Keto-PGF1a ratio may reflect increased PMNPLA2 activity. After treated with arachidonic acid (AA), a metabolite of PLA2 for 60min, the chemotaxis and adhesion of PMN were also significantly increased with the increase of TXB2 release. The PLA2 inhibitor PBPB can largely block the TNF-induced PMN chemotaxis and adhesion increase, while the epoxide enzyme inhibitor chlorobenzoylindoleacetic acid (IND) had no significant effect on TNF-induced PMN function. Activation of PLA2 may mediate the regulation of chemotaxis and adhesion of TNF to PMN. The use of PLA2 blockers may block the activation of TNF on PMN and reduce the body damage caused by inflammation.