Abstract
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- n ) treatment were described. The present study demonstrates that a 24 h treatment with IFN- n increases interleukin (IL)-6 release but reduces IL-8 secretion of both untreated and of tumor necrosis factor-alpha (TNF- f )-stimulated endothelial cells (ECs), favoring the attraction of lymphocytes but not of neutrophils. Alteration of cytokine release was accompanied by reduced basal and TNF- f -stimulated nuclear factor-kappa B (NF- s B) and activator protein-1 (AP-1) activity. However, IFN- n application neither altered gene expression of both TNF- f receptors (p55 and p75) nor cellular density of TNF- f receptor-2 (p75). Therefore, immune-modulatory action of IFN- n seems to be mediated by signal transduction molecules.