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Xenon modulates neutrophil adhesion molecule expression in vitro

Published online by Cambridge University Press:  23 December 2004

L. W. de Rossi
Affiliation:
University Hospital, Department of Anaesthesiology, Aachen, Germany
N. A. Horn
Affiliation:
University Hospital, Department of Anaesthesiology, Aachen, Germany
A. Stevanovic
Affiliation:
University Hospital, Department of Anaesthesiology, Aachen, Germany
W. Buhre
Affiliation:
University Hospital, Department of Anaesthesiology, Aachen, Germany
G. Hutschenreuter
Affiliation:
University Hospital, Institute of Transfusion Medicine, Aachen, Germany
R. Rossaint
Affiliation:
University Hospital, Department of Anaesthesiology, Aachen, Germany
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Abstract

Summary

Background and objective: Xenon reduces the infarct size after regional ischaemia in the rabbit heart in vivo, but the underlying mechanisms are unknown. Since adhesion molecules on neutrophils are closely involved in the pathophysiology of ischaemia/reperfusion injury and modulation of neutrophil function, we investigated the effect of xenon on neutrophil adhesion molecule expression in vitro.

Methods: Freshly isolated neutrophils were incubated with 30% or 60% xenon for 60 min. In unstimulated and after stimulation with either N-formyl-methionyl-leucyl-phenylalanine or phorbol-12-myristate-13-acetate neutrophil surface expression of PSGL-1, L-selectin, CD11a and CD11b were measured by flow cytometry.

Results: At both concentrations, xenon reduced the surface expression of PSGL-1 by 10% (P < 0.05), and of L-selectin by 15% (P < 0.05) in the 60% xenon group. Furthermore, N-formyl-methionyl-leucyl-phenylalanine activated neutrophils showed an increased removal of L-selectin from the neutrophil surface following incubation with xenon (30% compared to controls, P < 0.05). Neutrophil β2-integrin expression was not altered by xenon.

Conclusions: Xenon increases the removal of the selectins PSGL-1 and L-selectin from the neutrophil surface in vitro. Since both selectins are involved in the initial contact between neutrophils and endothelial cells, xenon may affect neutrophil adhesion to endothelium during ischaemia/reperfusion injury. However, because the β2-integrin expression was unaffected by xenon, further investigations are required to clarify whether xenon may modulate neutrophil transmigration through endothelial cells in vivo.

Type
Original Article
Copyright
2004 European Society of Anaesthesiology

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References

Collard CD, Gelman S. Pathophysiology, clinical manifestations, and prevention of ischemia–reperfusion injury. Anesthesiology 2001; 94: 11331138.Google Scholar
Cope DK, Impastato WK, Cohen MV, Downey JM. Volatile anesthetics protect the ischemic rabbit myocardium from infarction. Anesthesiology 1997; 86: 699709.Google Scholar
Heindl B, Reichle FM, Zahler S, Conzen PF, Becker BF. Sevoflurane and isoflurane protect the reperfused guinea pig heart by reducing postischemic adhesion of polymorphonuclear neutrophils. Anesthesiology 1999; 91: 521530.Google Scholar
Cason BA, Gamperl K, Slocum RE, Hickey RF. Anesthetic-induced preconditioning: previous administration of isoflurane decreases myocardial infarct size in rabbits. Anesthesiology 1997; 87: 11821190.Google Scholar
Preckel B, Müllenheim J, Moloschavij A, Thämer V, Schlack W. Xenon administration during early reperfusion reduces infarct size after regional ischemia in the rabbit heart in vivo. Anesth Analg 2000; 91: 13271332.Google Scholar
de Rossi LW, Horn NA, Baumert JH, Gutensohn K, Hutschenreuter G, Rossaint R. Xenon does not affect human platelet function in vitro. Anesth Analg 2001; 93: 635640.Google Scholar
de Rossi LW, Horn NA, Buhre W, Gass F, Hutschenreuter G, Rossaint R. Effect of isoflurane on neutrophil selectin and β2-integrin activation in vitro. Anesth Analg 2002; 95: 583587.Google Scholar
Sommerschild HT, Kirkeboen KA. Preconditioning-endogenous defence mechanisms of the heart. Acta Anaesthesiol Scand 2002; 46: 123137.Google Scholar
Vestweber D, Blanks JE. Mechanisms that regulate the function of the selectins and their ligands. Physiol Rev 1999; 79: 181213.Google Scholar
Davenpeck KL, Brummet ME, Hudson SA, Mayer RJ, Bochner BS. Activation of human leukocytes reduces surface P-selectin glycoprotein ligand-1 (PSGL-1, CD162) and adhesion to P-selectin in vitro. J Immunol 2000; 165: 27642772.Google Scholar
Kouki C, Beauchamp M, Baron C, Filep JG. Prevention of in vitro adhesion to endothelial cells through shedding of L-selectin by C-reactive protein and peptides derived from C-reactive protein. J Clin Invest 1997; 100: 522529.Google Scholar
Strausbaugh HJ, Green PG, Lo E, et al. Painful stimulation suppresses joint inflammation by inducing shedding of L-selectin from neutrophils. Nat Med 1999; 5: 1057.Google Scholar
Haribabu B, Steeber DA, Ali H, Richardson RM, Snyderman R, Tedder TF. Chemoattractant receptor-induced phosphorylation of L-selectin. J Biol Chem 1997; 272: 1396113965.Google Scholar
Alexander SR, Kishimoto TK, Walcheck B. Effects of selective protein kinase C inhibitors on the proteolytic down-regulation of L-selectin from chemoattractant-activated neutrophils. J Leukoc Biol 2000; 67: 415422.Google Scholar
Kahn J, Walcheck B, Migaki GI, Jutila MA, Kishimoto TK. Calmodulin regulates L-selectin adhesion molecule expression and function through a protease dependent mechanism. Cell 1998; 92: 809818.Google Scholar
Matala E, Alexander SR, Kishimoto TK, Walcheck B. The cytoplasmatic domain of L-selectin participates in regulating L-selectin endoproteolysis. J Immunol 2001; 167: 16171623.Google Scholar
Feehan C, Darlak K, Kahn J, Walcheck B, Spatola AF, Kishimoto TK. Shedding of lymphocyte L-selectin adhesion molecule is inhibited by a hydroxamic acid-based protease inhibitor. J Biol Chem 1996; 271: 70197024.Google Scholar
Lorant DE, McEver RP, McIntyre TM, Moore KL, Prescott SM, Zimmermann GA. Activation of polymorphonuclear leukocytes reduces their adhesion to P-selectin and causes redistribution of ligands for P-selectin on their surfaces. J Clin Invest 1995; 96: 171182.Google Scholar
Gardiner EE, De Luca M, McNally T, Michelson AD, Andrews RK, Berndt MC. Regulation of P-selectin binding to the neutrophil P-selectin counter-receptor P-selectin glycoprotein ligand-1 by neutrophil elastase and cathepsin G. Blood 2001; 98: 14401447.Google Scholar
Shang XZ, Issekutz AC. Contribution of CD11a/CD18, CD11b/CD18, ICAM-1 (CD54) and -2 (CD102) to human monocyte migration through endothelium and connective tissue fibroblast barriers. Eur J Immunol 1998; 28: 19701979.Google Scholar