Polytrauma induces increased expression of pyruvate kinase in neutrophils

Polytrauma (PT) leads to systemic activation of polymorphonuclear neutrophils (PMNs). Organ damage commonly found in these patients is ascribed to respiratory bursts of activated PMNs. With the use of sodium dodecyl sulfate–polyacrylamide gel electrophoresis, PMN extracts from PT patients were found...

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Bibliographic Details
Published in:Blood 2000-02, Vol.95 (3), p.1086-1092
Main Authors: Oehler, Rudolf, Weingartmann, Gertrude, Manhart, Nicole, Salzer, Ulrich, Meissner, Michael, Schlegel, Werner, Spittler, Andreas, Bergmann, Michael, Kandioler, Daniela, Oismüller, Christiane, Struse, Heidi M., Roth, Erich
Format: Article
Language:English
Subjects:
Adult
Aged
Biological and medical sciences
Cells, Cultured
Enzyme Induction
Female
Glycolysis
Humans
Lactic Acid - biosynthesis
Male
Medical sciences
Middle Aged
Multiple Organ Failure - enzymology
Multiple Organ Failure - etiology
Multiple trauma
Multiple Trauma - enzymology
Neutrophils - enzymology
Pyruvate Kinase - blood
Respiratory Burst
Time Factors
Traumas. Diseases due to physical agents
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Summary:Polytrauma (PT) leads to systemic activation of polymorphonuclear neutrophils (PMNs). Organ damage commonly found in these patients is ascribed to respiratory bursts of activated PMNs. With the use of sodium dodecyl sulfate–polyacrylamide gel electrophoresis, PMN extracts from PT patients were found to contain a clear protein band not seen in control PMNs from healthy volunteers. This band was identified by amino acid sequencing and Western blotting as pyruvate kinase (PK). Enzymatic assays revealed a 600-fold increase in PK activity in PMNs of PT patients, with the highest levels occurring between the fifth and seventh posttraumatic day. In lymphocytes, no such increase was detectable. As PK is a major regulatory enzyme in glycolysis, glucose-dependent lactate production in PMNs from PT patients was assayed. These cells showed a higher glycolytic lactate production than controls. It was additionally demonstrated that acute activation of respiratory burst activity depends mainly on breakdown of glucose to lactate via the pentose-phosphate pathway and glycolysis. In PMNs from PT patients, this glucose-dependent respiratory burst activity was more than twofold higher than in controls. The increase in expression and activity of PK in PMNs from PT patients may contribute to the high glucose-dependent respiratory burst activity seen in these cells.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V95.3.1086.003k09_1086_1092