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Leukocyte Aggregation Response to Quantitative Plasma Levels of C3a and C5a

Leukocyte Aggregation Response to Quantitative Plasma Levels of C3a and C5a Abstract • Granulocyte aggregation (GA) response has previously been described as a sensitive assay for complement activation in sepsis. Complement component C5a has been implicated as the plasma factor responsible for GA. The quantitative interaction of complement components C3a and C5a with GA, however, is not clearly defined. This study evaluates the relationship of GA responses to plasma levels of C5a and C3a in zymosan-activated plasma (ZAP). The C3a and C5a levels were measured by radioimmunoassay in serial dilutions of ZAP. Granulocyte aggregation responses of normal human leukocytes were determined for each ZAP dilution. The C5a levels in a 1:16 dilution of ZAP were higher than in normal plasma (22 ± 7 vs 9 ± 3 ng/mL), as were GA responses (24 ± 1 vs 11 ± 2 percentage of maximum light transmission). The C3a levels in a 1:8 dilution of ZAP are elevated above those of normal plasma (656±167 vs 411± 29 ng/mL). Correlation coefficients were .9809 for C3a vs GA, .9788 for C5a vs G, and .9860 for C3a vs C5a. Complement components C3a and C5a are involved in GA in vitro. Granulocyte aggregometry can detect low levels of activated complement in ZAP but may not be specific for C5a. The relative contribution of C3a and C5a to observed GA is not clear from the data. (Arch Surg 1986;121:305-307) References 1. Rinaldo JE, Rogers RM: Adult respiratory distress syndrome: Changing concepts of lung injury and repair . N Engl J Med 1982;306:900-909.Crossref 2. Jacob MS, Craddock OR, Hammerschmidt DE, et al: Complement-induced granulocyte aggregation: An unsuspected mechanism of disease . N Engl J Med 1980;302:789-794.Crossref 3. Solomkin JS, Simmons RL: Cellular and subcellular mediators of acute inflammation . Surg Clin North Am 1983;63:225-243. 4. Hammerschmidt DE, Weaver LJ, Hudson LD, et al: Association of complement activation and elevated plasma-C5a with adult respiratory distress syndrome . Lancet 1980;1:947-949.Crossref 5. Craddock PR, Hammerschmidt DE, White JG, et al: Complement (C5a)-induced granulocyte aggregation in vitro: A possible mechanism of complement-mediated leukostasis and leukopenia . J Clin Invest 1977;60: 260-264.Crossref 6. Chenowith DE, Hugli TE: Techniques and significance of C3a and C5a measurement , in Nakamura RM (ed): Future Perspectives in Clinical Laboratory Immunoassays . New York, Alan R Liss Inc, 1980, pp 443-459. 7. Solomkin JS, Cotta LA, Brodt JK, et al: Regulation of neutrophil superoxide production in sepsis . Arch Surg 1985;120:93-98.Crossref 8. Solomkin JS, Cotta LA, Ogle JD, et al: Complement-induced expression of cryptic receptors on the neutrophil surface: A mechanism for regulation of acute inflammation in trauma . Surgery 1984;96:336-344. 9. Hammerschmidt DE, Bowers TK, Lammi-Keefe CJ, et al: Granulocyte aggregometry: A sensitive technique for the detection of C5a and complement activation . Blood 1980;55:898-902. 10. Winer BJ: Statistical Principles in Experimental Design , ed 2. New York, McGraw-Hill International Book Co, 1971. 11. Heideman M, Hugli TE: Anaphylatoxin generation in multisystem organ failure . J Trauma 1984;24:1038-1043.Crossref 12. Slotman G, Burchard KW, Yellin SA, et al: Prostaglandin and complement interaction with clinical acute respiratory failure . Arch Surg 1986;121:271-274.Crossref 13. Chenowith DE, Hugli TE: Binding and degradation of C5a by human neutrophils , abstracted. J Immunol 1980;124:1517. 14. O'Flaherty JT, Showell HJ, Becker EL, et al: Substances which aggregate neutrophils: Mechanism of action . Am J Pathol 1978;92:155-166. 15. Hammerschmidt DE, White JH, Craddock PR, et al: Corticosteroids inhibit complement-induced granulocyte aggregation: A possible mechanism for their efficacy in shock state . J Clin Invest 1979;63:798-803.Crossref 16. O'Flaherty JT, Thomax MJ, Consart SL, et al: Neutropenia induced by systemic infusion of 5,12-dihydroxy-6,8,10,14-eicostatetraenoic acid: Correlation with its in vitro effects upon neutrophils . J Clin Invest 1982;69:993-998.Crossref 17. O'Flaherty JT, Kreutzer DL, Ward PA: Effect of prostaglandins E1, E2 and F2 on neutrophil aggregation . Prostaglandins 1979;17:201-210.Crossref 18. O'Flaherty JT, Showell MJ, Ward PA: A possible role of arachidonic acid in human neutrophil aggregation and degranulation . Am J Pathol 1979;96:799-810. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Surgery American Medical Association

Leukocyte Aggregation Response to Quantitative Plasma Levels of C3a and C5a

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References (19)

Publisher
American Medical Association
Copyright
Copyright © 1986 American Medical Association. All Rights Reserved.
ISSN
0004-0010
eISSN
1538-3644
DOI
10.1001/archsurg.1986.01400030059010
Publisher site
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Abstract

Abstract • Granulocyte aggregation (GA) response has previously been described as a sensitive assay for complement activation in sepsis. Complement component C5a has been implicated as the plasma factor responsible for GA. The quantitative interaction of complement components C3a and C5a with GA, however, is not clearly defined. This study evaluates the relationship of GA responses to plasma levels of C5a and C3a in zymosan-activated plasma (ZAP). The C3a and C5a levels were measured by radioimmunoassay in serial dilutions of ZAP. Granulocyte aggregation responses of normal human leukocytes were determined for each ZAP dilution. The C5a levels in a 1:16 dilution of ZAP were higher than in normal plasma (22 ± 7 vs 9 ± 3 ng/mL), as were GA responses (24 ± 1 vs 11 ± 2 percentage of maximum light transmission). The C3a levels in a 1:8 dilution of ZAP are elevated above those of normal plasma (656±167 vs 411± 29 ng/mL). Correlation coefficients were .9809 for C3a vs GA, .9788 for C5a vs G, and .9860 for C3a vs C5a. Complement components C3a and C5a are involved in GA in vitro. Granulocyte aggregometry can detect low levels of activated complement in ZAP but may not be specific for C5a. The relative contribution of C3a and C5a to observed GA is not clear from the data. (Arch Surg 1986;121:305-307) References 1. Rinaldo JE, Rogers RM: Adult respiratory distress syndrome: Changing concepts of lung injury and repair . N Engl J Med 1982;306:900-909.Crossref 2. Jacob MS, Craddock OR, Hammerschmidt DE, et al: Complement-induced granulocyte aggregation: An unsuspected mechanism of disease . N Engl J Med 1980;302:789-794.Crossref 3. Solomkin JS, Simmons RL: Cellular and subcellular mediators of acute inflammation . Surg Clin North Am 1983;63:225-243. 4. Hammerschmidt DE, Weaver LJ, Hudson LD, et al: Association of complement activation and elevated plasma-C5a with adult respiratory distress syndrome . Lancet 1980;1:947-949.Crossref 5. Craddock PR, Hammerschmidt DE, White JG, et al: Complement (C5a)-induced granulocyte aggregation in vitro: A possible mechanism of complement-mediated leukostasis and leukopenia . J Clin Invest 1977;60: 260-264.Crossref 6. Chenowith DE, Hugli TE: Techniques and significance of C3a and C5a measurement , in Nakamura RM (ed): Future Perspectives in Clinical Laboratory Immunoassays . New York, Alan R Liss Inc, 1980, pp 443-459. 7. Solomkin JS, Cotta LA, Brodt JK, et al: Regulation of neutrophil superoxide production in sepsis . Arch Surg 1985;120:93-98.Crossref 8. Solomkin JS, Cotta LA, Ogle JD, et al: Complement-induced expression of cryptic receptors on the neutrophil surface: A mechanism for regulation of acute inflammation in trauma . Surgery 1984;96:336-344. 9. Hammerschmidt DE, Bowers TK, Lammi-Keefe CJ, et al: Granulocyte aggregometry: A sensitive technique for the detection of C5a and complement activation . Blood 1980;55:898-902. 10. Winer BJ: Statistical Principles in Experimental Design , ed 2. New York, McGraw-Hill International Book Co, 1971. 11. Heideman M, Hugli TE: Anaphylatoxin generation in multisystem organ failure . J Trauma 1984;24:1038-1043.Crossref 12. Slotman G, Burchard KW, Yellin SA, et al: Prostaglandin and complement interaction with clinical acute respiratory failure . Arch Surg 1986;121:271-274.Crossref 13. Chenowith DE, Hugli TE: Binding and degradation of C5a by human neutrophils , abstracted. J Immunol 1980;124:1517. 14. O'Flaherty JT, Showell HJ, Becker EL, et al: Substances which aggregate neutrophils: Mechanism of action . Am J Pathol 1978;92:155-166. 15. Hammerschmidt DE, White JH, Craddock PR, et al: Corticosteroids inhibit complement-induced granulocyte aggregation: A possible mechanism for their efficacy in shock state . J Clin Invest 1979;63:798-803.Crossref 16. O'Flaherty JT, Thomax MJ, Consart SL, et al: Neutropenia induced by systemic infusion of 5,12-dihydroxy-6,8,10,14-eicostatetraenoic acid: Correlation with its in vitro effects upon neutrophils . J Clin Invest 1982;69:993-998.Crossref 17. O'Flaherty JT, Kreutzer DL, Ward PA: Effect of prostaglandins E1, E2 and F2 on neutrophil aggregation . Prostaglandins 1979;17:201-210.Crossref 18. O'Flaherty JT, Showell MJ, Ward PA: A possible role of arachidonic acid in human neutrophil aggregation and degranulation . Am J Pathol 1979;96:799-810.

Journal

Archives of Surgery – American Medical Association

Published: Mar 1, 1986

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