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Vol. 123 No. 2, February 1988 |
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PAPERS READ BEFORE THE SEVENTH ANNUAL MEETING OF THE SURGICAL INFECTION SOCIETY, PHILADELPHIA, MAY 11 TO MAY 12, 1987-PART I |
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Coagulation Augments Neutrophil C3b Receptors via Formation of a Protein(s) Unrelated to Fibrinolysis or C5 Activation
Julio Garcia-Aguilar, MD;
Marc E. Lanser, MD;
Glenn E. Brown, PhD
Arch Surg. 1988;123(2):199-203.
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 (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/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)
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.
Footnotes
Accepted for publication July 24, 1987.
Read before the Seventh Annual Meeting of the Surgical Infection Society, Philadelphia, May 11, 1987.
Reprint requests to Assistant Professor of Surgery, Beth Israel Hospital, 330 Brookline Ave, Boston, MA 02215 (Dr Lanser).
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