Transient exposure of human eosinophils to the protein kinase C inhibitors CGP39-360, CGP41-251, and CGP44-800 leads to priming of the respiratory burst induced by opsonized particles

T. Van der Bruggen, P. T.M. Kok, M. Blom, A. J. Verhoeven, J. A.M. Raaijmakers, J. W.J. Lammers, L. Koenderman*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

15 Citations (Scopus)

Abstract

We report that a transient incubation of human eosinophils with the protein kinase C (PKC) inhibitor CGP39-360 (staurosporine) or the more PKC- specific inhibitors CGP41-251 and CGP44-800 prior to activation of the respiratory burst with opsonized particles results in priming of this response. This priming effect was concentration dependent and occurred in the range in which the phorbol myristate acetate-induced respiratory burst was inhibited. CGP39-360 priming was minimally affected in Ca2+-depleted cells, indicating that an increase in [Ca2+](i) is not important. Also, the binding of serum-treated zymosan (STZ) particles was strongly enhanced by the inhibitors. On the other hand, the release of platelet-activating factor (PAF) induced by opsonized particles was enhanced only by CGP39-360 and not by CGP41-251 and CGP44-800. Therefore, priming of the respiratory burst is not due to an aspecific enhancing effect of the inhibitors. These data indicate that different signal transduction routes are involved in priming of the STZ-induced respiratory burst and PAF release in human eosinophils.

Original languageEnglish
Pages (from-to)552-557
Number of pages6
JournalJournal of Leukocyte Biology
Volume54
Issue number6
DOIs
Publication statusPublished - 1 Jan 1993

Keywords

  • eosinophils
  • opsonized particles
  • PKC inhibitors
  • respiratory burst

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