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Endogenous Adenosine Formation can Regulate Human Neutrophil Function

  • Jerzy Barankiewicz
  • Roland Jimenez
  • Jon Uyesaka
  • Elisabeth Colmerauer
  • Gary S. Firestein
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 370)

Abstract

Neutrophils, in addition to their role in host defense, can cause injury to normal tissues during inflammatory processes. Oxygen radicals and secreted proteases, in particular, are responsible for some aspects of neutrophil-mediated injury to endothelial cells and cardiomyocytes. A variety of neutrophil functions, including adhesion and reactive oxygen species production, are inhibited by adenosine (Ado) (Cronstein, 1991 and Cronstein, et al., 1992). Furthermore, inhibition of neutrophil adhesion by adenosine regulating agents like acadesine and adenosine kinase (AK) inhibitors (Firestein, et al., 1994) appears to be mediated by Ado, since it is reversed by the addition of adenosine deaminase (ADA) or Ado receptor antagonists. Although Ado and adenine nucleotides can be released at inflammatory sites during platelet aggregation or from endothelial cells during ischemic stress conditions, little is known about Ado formation by human neutrophils. To determine if neutrophils can serve as an endogenous Ado source and thereby provide an autocrine stimulus, we evaluated purine metabolism and Ado formation in human neutrophils.

Keywords

Human Neutrophil Adenine Nucleotide Adenosine Deaminase Neutrophil Adhesion Adenosine Kinase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Cronstein, B.N., Purines and inflammation: Neutrophils possess P1 and P2 purine receptors, in: “Adenosine and Adenine Nucleotides as Regulators of Cellular function,” J.W. Phillis, ed., CRC Press, Boca Raton (1991).Google Scholar
  2. 2.
    Cronstein, B.N., Levin R.L, Philips, M, Hirschhorn, R., Abramson, S.B., and Weissmann, G., Neutrophil adherence to endothelium is enhanced via adenosine A1 receptors and inhibited via adenosine A2 receptors, J. Immunol. 148: 2201 (1992).PubMedGoogle Scholar
  3. 3.
    Firestein, G.S., Bullough, D.A., Erion, M.D., Jimenez, R., Ramirez-Weinhouse, M., Barankiewicz, J., Smith., C.W., Gruber, H.E., and Mullane, K.M., Inhibition of neutrophil adhesion by adenosine and an adenosine kinase inhibitor: The role of selectins, submitted for publication.Google Scholar

Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • Jerzy Barankiewicz
    • 1
  • Roland Jimenez
    • 1
  • Jon Uyesaka
    • 1
  • Elisabeth Colmerauer
    • 1
  • Gary S. Firestein
    • 1
  1. 1.Gensia, Inc.San DiegoUSA

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