[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.197.142.219. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Article
February 1988

Coagulation Augments Neutrophil C3b Receptors via Formation of a Protein(s) Unrelated to Fibrinolysis or C5 Activation

Author Affiliations

From the Longwood Area Trauma Center (Dr Lanser) and the Departments of Surgery (Drs Garcia-Aguilar and Lanser) and Biological Chemistry (Dr Brown), Beth Israel Hospital, Harvard Medical School, Boston.

Arch Surg. 1988;123(2):199-203. doi:10.1001/archsurg.1988.01400260083010
Abstract

• 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 (×3.43±0.93) and CR3 (×3.07 ±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/106 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 Xlla, were shown not to be responsible for this CR-inducing activity.

(Arch Surg 1988;123:199-203)

×