Abstract
Products of C-activation (particularly C5a) induce chemotaxis, phagocytosis, and lysosomal exocytosis by GR, and thus profoundly influence the role of GR in inflammation. We have recently reported that C5a will induce GR aggregation in vitro. This aggregation is specifically dependent on C5a in that aggregating activity can be generated in normal but not C5-deficient plasma by incubation with zymosan (ZYM); the aggregating activity in normal ZYM-treated plasma is limited to a single peak of 17,000 daltons, is heat stable (56° × 30 min), and is inhibited by incubation with anti-C5 but not anti-C3 antisera. The amplitude of the aggregator response is proportional to log2 [C5a]. GR aggregation might therefore be used as an assay for C5a and thus for C activation. The aggregation response of GR to C5a is amplified tenfold by the addition of cytochalasin B (CB).
