Borgmann S, Bayer A, König W, Ambrosch A, Kraus J
Institute of Medical Microbiology, Eberhard-Karl-University of Tübingen, Germany.
Endothelium. 2002;9(3):173-8. doi: 10.1080/10623320213636.
The benefit of neutrophil exclusion from type 1 T helper cell (TH1) inflammatory processes was demonstrated in clinical studies. Increased recruitment of lymphocytes and monocytes to endothelium and impaired recruitment of polymorphonuclear neutrophils (PMNs) following interferon-gamma (IFN-gamma) treatment were described. The present study demonstrates that a 24 h treatment with IFN-gamma increases interleukin (IL)-6 release but reduces IL-8 secretion of both untreated and of tumor necrosis factor-alpha (TNF-alpha)-stimulated endothelial cells (ECs), favoring the attraction of lymphocytes but not of neutrophils. Alteration of cytokine release was accompanied by reduced basal and TNF-alpha-stimulated nuclear factor-kappa B (NF-kappa B) and activator protein-1 (AP-1) activity. However, IFN-gamma application neither altered gene expression of both TNF-alpha receptors (p55 and p75) nor cellular density of TNF-alpha receptor-2 (p75). Therefore, immune-modulatory action of IFN-gamma seems to be mediated by signal transduction molecules.
临床研究证明了嗜中性粒细胞从1型辅助性T细胞（TH1）炎症过程中被排除的益处。研究描述了干扰素-γ（IFN-γ）治疗后淋巴细胞和单核细胞向内皮的募集增加以及多形核中性粒细胞（PMN）的募集受损。本研究表明，用IFN-γ进行24小时治疗可增加白细胞介素（IL）-6的释放，但会降低未处理的以及肿瘤坏死因子-α（TNF-α）刺激的内皮细胞（EC）的IL-8分泌，有利于淋巴细胞而非嗜中性粒细胞的吸引。细胞因子释放的改变伴随着基础和TNF-α刺激的核因子-κB（NF-κB）及活化蛋白-1（AP-1）活性的降低。然而，IFN-γ的应用既未改变两种TNF-α受体（p55和p75）的基因表达，也未改变TNF-α受体-2（p75）的细胞密度。因此，IFN-γ的免疫调节作用似乎是由信号转导分子介导的。
