Thrombospondin-exposed human monocytes display augmented luminol-enhanced chemiluminescence upon receptor triggering.

It was tested whether the exposure to blood platelet thrombospondin (TSP) influences the function of monocytes. TSP-treated monocytes displayed luminol-enhanced chemiluminescence (CL) upon triggering with polyclonal or monoclonal anti-TSP. This response was mediated by an Fc receptor, since F(ab')2 fragments were without effect. Evidence is provided that a CL signal was induced only when antibodies bound to TSP and Fc receptors of the same monocyte. TSP-treated monocytes exerted enhanced CL to aggregated IgG when compared with untreated or albumin-treated cells, suggesting that TSP up-regulated the cells' capacity to mediate Fc receptor-dependent generation of reactive oxygen. A similar enhancement was observed when TSP-treated cells were stimulated with anti-CD36, or with fMLP. Upon stimulation of TSP-pretreated cells with monoclonal anti-fibrinogen (Fg), a much stronger enhancement was noted, which was similar in magnitude to that induced by anti-TSP. The effect of anti-Fg cannot be explained by a trace contamination of TSP with Fg alone. In contrast to receptor-mediated CL, PMA-induced and zymosan-induced CL were influenced little by TSP pretreatment. IgG-mediated phagocytosis was not enhanced in TSP-treated cells. Thus, TSP selectively modulates certain monocyte functions which could be of physiological relevance.