Coagulation augments neutrophil C3b receptors via formation of a protein(s) unrelated to fibrinolysis or C5 activation

J. Garcia-Aguilar, M. E. Lanser and G. E. Brown
Department of Surgery, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215.

The present study investigated the effect of coagulation on neutrophil complement receptors (CRs) 1 and 3, which are specific for the opsonins C3b and C3bi. Incubation of neutrophils in autologous serum, but not in plasma, increased the mean (+/- SD) expression of CR1 (x3.43 +/- 0.93) and CR3 (x3.07 +/- 0.86), in comparison with incubation in buffer. Serum also increased neutrophil superoxide production in response to opsonized zymosan from 0.48 +/- 0.21 to 1.05 +/- 0.25 nmol/10(6) cells/min. Similarly, calcium conversion of platelet-rich plasma (but not platelet-poor plasma) to serum also increased both CR1 and CR3 expression. This finding, as well as the fact that freeze-thawed platelet-rich plasma (but not platelet-poor plasma) increased CR expression, indicated that platelet constituents were the origin of this CR-inducing activity. Other nonplatelet factors formed during coagulation, such as C5a, fibrinogen degradation products, kallikrein, and factor XIIa, were shown not to be responsible for this CR-inducing activity.